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Cancer immunotherapy has emerged as a promising strategy for the treatment of cancer, with the tumor microenvironment (TME) playing a pivotal role in modulating the immune response. CD47, a cell surface protein, has been identified as a crucial regulator of the TME and a potential therapeutic target for cancer therapy. However, the precise functions and implications of CD47 in the TME during immunotherapy for cancer patients remain incompletely understood. This comprehensive review aims to provide an overview of CD47's multifaced role in TME regulation and immune evasion, elucidating its impact on various types of immunotherapy outcomes, including checkpoint inhibitors and CAR T-cell therapy. Notably, CD47-targeted therapies offer a promising avenue for improving cancer treatment outcomes, especially when combined with other immunotherapeutic approaches. The review also discusses current and potential CD47-targeted therapies being explored for cancer treatment and delves into the associated challenges and opportunities inherent in targeting CD47. Despite the demonstrated effectiveness of CD47-targeted therapies, there are potential problems, including unintended effects on healthy cells, hematological toxicities, and the development if resistance. Consequently, further research efforts are warranted to fully understand the underlying mechanisms of resistance and to optimize CD47-targeted therapies through innovative combination approaches, ultimately improving cancer treatment outcomes. Overall, this comprehensive review highlights the significance of CD47 as a promising target for cancer immunotherapy and provides valuable insight into the challenges and opportunities in developing effective CD47-targeted therapies for cancer treatment.

Simple Summary: In managing cancer diseases, emerging tools and technologies are pivotal for stakeholders including basic scientists, preclinicians, clinicians, and health data managers. In recent years, the emergence of artificial intelligence (AI)-based tools and programs has helped in significant ways to achieve holistic approaches including the diagnosis, therapy, and prognosis of cancer patients. It is true that in achieving enhanced management of cancer patients, productivity in terms of various forms of data, research publications, and patents centered on oncology has increased many-fold. Besides the positive impact of AI on cancer patients and involved stakeholders, reliable balanced approaches are also needed at the moment so that issues of ethics such as patient privacy and data bias can be resolved. Also, the future influence of AI on the creative and disruptive abilities of involved researchers is safeguarded by policies and guidelines on the extent of its uses in oncology. Artificial intelligence (AI), encompassing several tools and platforms such as artificial "general" intelligence (AGI) and generative artificial intelligence (GenAI), has facilitated cancer research, enhancing productivity in terms of research publications and translational value for cancer patients. AGI tools, such as ChatGPT, assist preclinical and clinical scientists in identifying tumor heterogeneity, predicting therapy outcomes, and streamlining research publications. However, this perspective review also explores the potential of AI's influence on cancer research with regard to its impact on disruptive sciences and discoveries by preclinical and clinical scientists. The increasing reliance on AI tools may compromise biological intelligence, disrupting abstraction, creativity, and critical thinking. This could contribute to the declining trend of disruptive sciences, hindering landmark discoveries and innovations. This perspective review narrates the role of different forms of AI in the potentiation of productive cancer research and the potential disruption of disruptive sciences due to AI's influence. [ABSTRACT FROM AUTHOR]

In this study, a D‐shaped, extremely sensitive surface plasmon resonance (SPR) sensor with a blue shift characteristic is proposed that can be used to identify various malignant cancer cells. A sensing layer made of titanium is inserted to produce intense sensitivity. For the simulation and numerical evaluation of the proposed biosensor, we used the finite element method (FEM) and the COMSOL Multiphysics 5.6 software. To regulate how much light passes through the sensor, which incites the released electrons at the surface of the plasmonic material, air holes in different radii are used. The characteristics that make our proposed sensor superior to other D‐shaped SPR sensors are—it gives an excellent amplitude sensitivity (AS) of 200 RIU−1 also ensures extremely high wavelength sensitivity (WS) spanning from 34,350 to 42,145 nm/RIU with an outstanding spectral resolution of 2.37 × 10−6 RIU. Furthermore, the R2 (0.9966) value is also extremely close to 1 which ensures the quality of our sensor regarding its performance. The given sensor is tailored for four vital human cancers, which are blood cancer, skin cancer, cervical cancer, and adrenal gland cancer. Here, optimization of the structural geometric parameters, plasmonic materials, and material thickness are also conducted in search of the best functionality of the sensor. The offered structure, nonetheless, can be an obvious prologue in the case of the crucial human cancer detection platform due to its mild sensing performances. [ABSTRACT FROM AUTHOR]

The Hippo signaling pathway has a regulatory function in the organogenesis process and cellular homeostasis, switching the cascade reactions of crucial kinases acts to turn off/on the Hippo pathway, altering the downstream gene expression and thereby regulating proliferation, apoptosis, or stemness. Disruption of this pathway can lead to the occurrence of various disorders and different types of cancer. Recent findings highlight the importance of ncRNAs, such as microRNA, circular RNA, and lncRNAs, in modulating the Hippo pathway. Defects in ncRNAs can disrupt Hippo pathway balance, increasing tumor cells, tumorigenesis, and chemotherapeutic resistance. This review summarizes ncRNAs' inhibitory or stimulatory role in - Hippo pathway regulation in cancer and stem cells. Identifying the relation between ncRNAs and the components of this pathway could pave the way for developing new biomarkers in the treatment and diagnosis of cancers.

Photodynamic therapy (PDT) can not only directly eliminate cancer cells, but can also stimulate antitumor immune responses. It also affects the expression of immune checkpoints. The purpose of this review is to collect, analyze, and summarize recent news about PDT and immune checkpoints, along with their inhibitors, and to identify future research directions that may enhance the effectiveness of this approach. A search for research articles published between January 2023 and March 2024 was conducted in PubMed/MEDLINE. Eligibility criteria were as follows: (1) papers describing PDT and immune checkpoints, (2) only original research papers, (3) only papers describing new reports in the field of PDT and immune checkpoints, and (4) both in vitro and in vivo papers. Exclusion criteria included (1) papers written in a language other than Polish or English, (2) review papers, and (3) papers published before January 2023. 24 papers describing new data on PDT and immune checkpoints have been published since January 2023. These included information on the effects of PDT on immune checkpoints, and attempts to associate PDT with ICI and with other molecules to modulate immune checkpoints, improve the immunosuppressive environment of the tumor, and resolve PDT-related problems. They also focused on the development of new nanoparticles that can improve the delivery of photosensitizers and drugs selectively to the tumor. The effect of PDT on the level of immune checkpoints and the associated activity of the immune system has not been fully elucidated further, and reports in this area are divergent, indicating the complexity of the interaction between PDT and the immune system. PDT-based strategies have been shown to have a beneficial effect on the delivery of ICI to the tumor. The utility of PDT in enhancing the induction of the antitumor response by participating in the triggering of immunogenic cell death, the exposure of tumor antigens, and the release of various alarm signals that together promote the activation of dendritic cells and other components of the immune system has also been demonstrated, with the result that PDT can enhance the antitumor immune response induced by ICI therapy. PDT also enables multifaceted regulation of the tumor’s immunosuppressive environment, as a result of which ICI therapy has the potential to achieve better antitumor efficacy. The current review has presented evidence of PDT’s ability to modulate the level of immune checkpoints and the effectiveness of the association of PDT with ICIs and other molecules in inducing an effective immune response against cancer cells. However, these studies are at an early stage and many more observations need to be made to confirm their efficacy. The new research directions indicated may contribute to the development of further strategies.

Cancer cells refer to a group of malignant cells with strong division and proliferation abilities. Cancer cells rely on the unstable plunder of human nutrition to sustain the large amount of energy that they need for their own division and proliferation. The division and proliferation of cancer cells are linked to the synthesis and replication of genetic material in the nucleus. Blockage or destruction of the synthesis of genetic material in cancer cells is one of the mechanisms underlying the action of most antitumor drugs. As the key material that dominates cell division, proliferation, and death, nuclear genetic material which mainly refers to the deoxyribonucleic acid located on the chromatin in the nucleus, plays a decisive role in the final fate of cells. The final fate of cancer cells after the damage of the genetic material is worthy of investigation and analysis. In this paper, we discuss and analyze the fate of cancer cells after genetic material damage from the aspect of cellular cycle arrest, apoptosis, autophagy, and senescence to provide ideas for the mechanism research on antitumor drugs.

Abstract Entrapping phytochemical bioactive compounds into nano-structured biocompatible polymers has been successfully utilized for improving cancer treatment efficiency. Silibinin is a potent compound that shows promising anticancer properties. In the present study, the Zein-β-cyclodextrin complex was used to encapsulate silibinin and evaluate the induced cell death type and cytotoxic impacts on human cancer cells. The silibinin-loaded Zein-β cyclodextrin nano-carriers (SZBC-NCs) were synthesized utilizing a gradual ultrasound-mediated homogenization technique and characterized by Zeta potential, DLS, FESEM, and FTIR analysis. The SZBC-NCs’ antioxidant activity was studied by conducting ABTS and DPPH radical scavenging assays. Finally, the SZBC-NCs selective toxicity and cellular death induction mechanism were studied on the HT-29 and AGS cancer cells by measuring the cell survival and apoptotic gene (Caspase 3, 9), respectively, which were verified by conducting the DAPI staining analysis. The negatively charged (− 27.47 mV) nanoparticles (286.55 nm) showed significant ABTS and DPPH radical scavenging activity. Moreover, the remarkable decrease in the IC50 concentrations of the SZBC-NCs among the HT-29 and AGS cancer cell lines exhibited their selective cytotoxic potential. Also, the overexpressed apoptotic (Caspases 3 and 9) and down-regulated necrotic (NFKB) gene expressions following the SZBC-NCs treatment doses indicated the apoptotic activity of SZBC-NCs, which were verified by the increased apoptotic morphology of the DAPI-stained HT-29 cancer cells. The antioxidant and colon cancer cell-related apoptotic activity of the SZBC-NCs make it an appropriate anti-colon cancer nano delivery system. Therefore, they can potentially be used as a safe efficient colon cancer treatment strategy. However, further in vivo experiments including animal cancer models have to be studied.

Abstract Macrophages infiltrating tumour tissues or residing in the microenvironment of solid tumours are known as tumour-associated macrophages (TAMs). These specialized immune cells play crucial roles in tumour growth, angiogenesis, immune regulation, metastasis, and chemoresistance. TAMs encompass various subpopulations, primarily classified into M1 and M2 subtypes based on their differentiation and activities. M1 macrophages, characterized by a pro-inflammatory phenotype, exert anti-tumoural effects, while M2 macrophages, with an anti-inflammatory phenotype, function as protumoural regulators. These highly versatile cells respond to stimuli from tumour cells and other constituents within the tumour microenvironment (TME), such as growth factors, cytokines, chemokines, and enzymes. These stimuli induce their polarization towards one phenotype or another, leading to complex interactions with TME components and influencing both pro-tumour and anti-tumour processes. This review comprehensively and deeply covers the literature on macrophages, their origin and function as well as the intricate interplay between macrophages and the TME, influencing the dual nature of TAMs in promoting both pro- and anti-tumour processes. Moreover, the review delves into the primary pathways implicated in macrophage polarization, examining the diverse stimuli that regulate this process. These stimuli play a crucial role in shaping the phenotype and functions of macrophages. In addition, the advantages and limitations of current macrophage based clinical interventions are reviewed, including enhancing TAM phagocytosis, inducing TAM exhaustion, inhibiting TAM recruitment, and polarizing TAMs towards an M1-like phenotype. In conclusion, while the treatment strategies targeting macrophages in precision medicine show promise, overcoming several obstacles is still necessary to achieve an accessible and efficient immunotherapy.

Ultrasound examination is becoming the most popular medical imaging modality because of its low cost and high safety profile. Ultrasound contrast agents enhance the scattering of sound waves, which can improve the clarity and resolution of images. Nanoparticle Ultrasound contrast agents have the characteristics of a large specific surface area and a modifiable surface, which can increase drug loading capacity, prolong circulation time, and enable drug enrichment in specific organs or tissues. This leads to improved therapeutic effects and reducing toxic and side effects. Compared with traditional ultrasound contrast agents, Nano-ultrasound contrast agents overcome the limitation of imaging solely within blood vessels and facilitate imaging within tumor tissues, thereby extending the duration of enhanced imaging. Sonodynamic therapy is an emerging treatment method that has been developed rapidly in recent years, which has the advantages of noninvasive, high spatial and temporal resolution, and low toxicity and side effects. Sonodynamic therapy utilizes a sonosensitizer that, when excited by ultrasound at the tumor site, produces toxic reactive oxygen species, inducing apoptosis or necrosis in tumor cells. Ultrasound-guided sonodynamic therapy allows for real-time observation of lesions, is convenient and flexible, and is free of radiation exposure. With the use of nanomaterials as carriers, ultrasound-guided sonodynamic therapy has made significant strides. This study categorizes and summarizes the current research on acoustic sensitizer carrier materials, including carbon-based, silicon-based, peptide-based, iron-based, metal-organic frameworks, polymers, and liposomes. It concludes by highlighting the current challenges in the integration of ultrasound imaging with sonodynamic therapy and suggests future directions for clinical application development. [ABSTRACT FROM AUTHOR]

Osteosarcoma is a common malignancy that often occurs in children, teenagers and young adults. Although the treatment strategy has improved, the results are still poor for most patients with metastatic or recurrent osteosarcomas. Therefore, it is necessary to identify new and effective prognostic biomarkers and therapeutic targets for diseases. Human genomes contain lncRNAs, transcripts with limited or insufficient capacity to encode proteins. They have been implicated in tumorigenesis, particularly regarding the onset, advancement, resistance to treatment, recurrence and remote dissemination of malignancies. Aberrant lncRNA expression in osteosarcomas has been reported by numerous researchers; lncRNAs have the potential to exhibit either oncogenic or tumorsuppressing behaviors and thus, to govern the advancement of this skeletal cancer. They are suspected to influence osteosarcoma cell growth, replication, invasion, migration, remote dissemination and programmed cell death. Additionally, they have been recognized as clinical markers, and may participate in the development of multidrug resistance. Therefore, the study of lncRNAs in the growth, metastasis, treatment and prognosis of osteosarcoma is very important for the active prevention and treatment of osteosarcoma. Consequently, this work reviews the functions of lncRNAs. [ABSTRACT FROM AUTHOR]

Nanosecond pulsed electric fields (nsPEFs) have recently shown promise as a cancer therapy. Although nsPEF‐induced apoptotic responses have been observed, the stress on individual cell components has not been quantified. Therefore, the authors built a cell equivalent circuit, including mitochondria, to quantitatively calculate the voltage, electric field, and electrical energy applied to the cell components in the frequency domain. Additionally, pulse width and electrical energy changed in mitochondrial membrane potential over time. The results indicated that the change of pulsed voltage switched the cell stimulation pathway, resulting in different mitochondrial membrane potentials over time. The frequency response analysis confirmed that the potential on mitochondrial membranes increased under shorter pulse width conditions. This suggested that the frequency analysis provided in this paper is useful for relating the site of cellular stimulation to induce physiological effects. © 2024 Institute of Electrical Engineers of Japan and Wiley Periodicals LLC. [ABSTRACT FROM AUTHOR]

Cancer cells refer to a group of malignant cells with strong division and proliferation abilities. Cancer cells rely on the unstable plunder of human nutrition to sustain the large amount of energy that they need for their own division and proliferation. The division and proliferation of cancer cells are linked to the synthesis and replication of genetic material in the nucleus. Blockage or destruction of the synthesis of genetic material in cancer cells is one of the mechanisms underlying the action of most antitumor drugs. As the key material that dominates cell division, proliferation, and death, nuclear genetic material which mainly refers to the deoxyribonucleic acid located on the chromatin in the nucleus, plays a decisive role in the final fate of cells. The final fate of cancer cells after the damage of the genetic material is worthy of investigation and analysis. In this paper, we discuss and analyze the fate of cancer cells after genetic material damage from the aspect of cellular cycle arrest, apoptosis, autophagy, and senescence to provide ideas for the mechanism research on antitumor drugs. [ABSTRACT FROM AUTHOR]

In this study, we evaluated the cancer cell killing activity of koji mold-derived extracts using several solvents. The koji mold lipid extract (KML) exhibited potent cytotoxicity against a human leukemia cell line. Fractionation of the KML via silica gel chromatography revealed the presence of active components in fraction (Fr.) 6. Cytotoxic effects of Fr. 6 were inhibited by the ferroptosis inhibitors, ferrostatin-1 and SRS11-92, and the iron chelator, deferoxamine. Interestingly, ferroptosis inhibitors failed to prevent the KML-induced cell death. Fr. 6 decreased the expression of glutathione peroxidase 4 (GPx4) and increased the level of peroxidized plasma membrane lipids. Furthermore, Fr. 6 decreased the intracellular glutathione levels. Overall, our results suggest that Fr. 6 included in KML induces ferroptosis in HL-60 cells. [ABSTRACT FROM AUTHOR]

Entrapping phytochemical bioactive compounds into nano-structured biocompatible polymers has been successfully utilized for improving cancer treatment efficiency. Silibinin is a potent compound that shows promising anticancer properties. In the present study, the Zein-β-cyclodextrin complex was used to encapsulate silibinin and evaluate the induced cell death type and cytotoxic impacts on human cancer cells. The silibinin-loaded Zein-β cyclodextrin nano-carriers (SZBC-NCs) were synthesized utilizing a gradual ultrasound-mediated homogenization technique and characterized by Zeta potential, DLS, FESEM, and FTIR analysis. The SZBC-NCs' antioxidant activity was studied by conducting ABTS and DPPH radical scavenging assays. Finally, the SZBC-NCs selective toxicity and cellular death induction mechanism were studied on the HT-29 and AGS cancer cells by measuring the cell survival and apoptotic gene (Caspase 3, 9), respectively, which were verified by conducting the DAPI staining analysis. The negatively charged (− 27.47 mV) nanoparticles (286.55 nm) showed significant ABTS and DPPH radical scavenging activity. Moreover, the remarkable decrease in the IC50 concentrations of the SZBC-NCs among the HT-29 and AGS cancer cell lines exhibited their selective cytotoxic potential. Also, the overexpressed apoptotic (Caspases 3 and 9) and down-regulated necrotic (NFKB) gene expressions following the SZBC-NCs treatment doses indicated the apoptotic activity of SZBC-NCs, which were verified by the increased apoptotic morphology of the DAPI-stained HT-29 cancer cells. The antioxidant and colon cancer cell-related apoptotic activity of the SZBC-NCs make it an appropriate anti-colon cancer nano delivery system. Therefore, they can potentially be used as a safe efficient colon cancer treatment strategy. However, further in vivo experiments including animal cancer models have to be studied. [ABSTRACT FROM AUTHOR]

Macrophages infiltrating tumour tissues or residing in the microenvironment of solid tumours are known as tumour-associated macrophages (TAMs). These specialized immune cells play crucial roles in tumour growth, angiogenesis, immune regulation, metastasis, and chemoresistance. TAMs encompass various subpopulations, primarily classified into M1 and M2 subtypes based on their differentiation and activities. M1 macrophages, characterized by a pro-inflammatory phenotype, exert anti-tumoural effects, while M2 macrophages, with an anti-inflammatory phenotype, function as protumoural regulators. These highly versatile cells respond to stimuli from tumour cells and other constituents within the tumour microenvironment (TME), such as growth factors, cytokines, chemokines, and enzymes. These stimuli induce their polarization towards one phenotype or another, leading to complex interactions with TME components and influencing both pro-tumour and anti-tumour processes. This review comprehensively and deeply covers the literature on macrophages, their origin and function as well as the intricate interplay between macrophages and the TME, influencing the dual nature of TAMs in promoting both pro- and anti-tumour processes. Moreover, the review delves into the primary pathways implicated in macrophage polarization, examining the diverse stimuli that regulate this process. These stimuli play a crucial role in shaping the phenotype and functions of macrophages. In addition, the advantages and limitations of current macrophage based clinical interventions are reviewed, including enhancing TAM phagocytosis, inducing TAM exhaustion, inhibiting TAM recruitment, and polarizing TAMs towards an M1-like phenotype. In conclusion, while the treatment strategies targeting macrophages in precision medicine show promise, overcoming several obstacles is still necessary to achieve an accessible and efficient immunotherapy. [ABSTRACT FROM AUTHOR]

Introduction: Oral Squamous Cell Carcinoma (OSCC) is a prevalent form of oral cancer, ranking 17th in prevalence in Indonesia. It is typically managed through surgical procedures, chemotherapy, and radiotherapy, though these interventions may adversely impact patients' quality of life. Additionally, OSCC often exhibits resistance to conventional drugs, prompting research into potential and effective anticancer therapies, particularly targeting the epidermal growth factor receptor (EGFR). Qusthul hindi (Saussurea costus), commonly known as qust, is a biopharmaceutical plant native to South Asia. It is extensively employed for medicinal purposes, especially its root extracts, known for their high concentration of sesquiterpene compounds, which demonstrate notable anticancer properties. Objectives: To predict the potential of sesquiterpene compound of qust extract (SCoQE) as anticancer therapy in inhibiting EGFR. Materials and methods: The study design is descriptive, using an in silico method involving computational prediction. It consists of several stages, including preparation, PASS prediction test, physicochemical tests, ADMET prediction, and molecular docking simulation. Results: SCoQE exhibits distinct anticancer properties against OSCC by effectively inhibiting the active site of EGFR. Additionally, SCoQE demonstrates drug-like characteristics, with a considerable likelihood (probability greater than 0.700) of acting as an anticancer agent. Furthermore, SCo-QE is anticipated to be adequately absorbed and distributed throughout the body during the initial metabolic pass, with a predicted absence of toxic effects. Conclusion: SCoQE has ability to inhibit EGFR with the most promising compound being costunolide and dehydrocostus lactone. In further studies will be carried out other comprehensive studies to mapping anticancer ability. [ABSTRACT FROM AUTHOR]

Autophagy is a globally conserved cellular activity that plays a critical role in maintaining cellular homeostasis through the breakdown and recycling of cellular constituents. In recent years, there has been much emphasis given to its complex role in cancer stem cells (CSCs) and stem cell treatment. This study examines the molecular processes that support autophagy and how it is regulated in the context of CSCs and stem cell treatment. Although autophagy plays a dual role in the management of CSCs, affecting their removal as well as their maintenance, the intricate interaction between the several signaling channels that control cellular survival and death as part of the molecular mechanism of autophagy has not been well elucidated. Given that CSCs have a role in the development, progression, and resistance to treatment of tumors, it is imperative to comprehend their biological activities. CSCs are important for cancer biology because they also show a tissue regeneration model that helps with organoid regeneration. In other words, the manipulation of autophagy is a viable therapeutic approach in the treatment of cancer and stem cell therapy. Both synthetic and natural substances that target autophagy pathways have demonstrated promise in improving stem cell-based therapies and eliminating CSCs. Nevertheless, there are difficulties associated with the limitations of autophagy in CSC regulation, including resistance mechanisms and off-target effects. Thus, the regulation of autophagy offers a versatile strategy for focusing on CSCs and enhancing the results of stem cell therapy. Therefore, understanding the complex interactions between autophagy and CSC biology would be essential for creating therapeutic treatments that work in both regenerative medicine and cancer treatment. [ABSTRACT FROM AUTHOR]

Three-dimensional cell culture spheroids are commonly used for drug evaluation studies because they can produce large quantities of homogeneous cell aggregates. As the spheroids grow, nutrients supplied from outer spheroid regions render the inner spheroid areas hypoxic and hyponutrient, which makes them unobservable through confocal microscopy. In this study, we fabricated a cancer cell aggregate culture device that facilitates the observation of nutrient and oxygen gradients. An alginate gel fiber was created in the cell culture chamber to ensure a flow path for supplying the culture medium. A gradient of nutrients and oxygen was generated by positioning the flow channel close to the edge of the chamber. We devised a fabrication method that uses calcium carbonate as a source of Ca2+ for the gelation of sodium alginate, which has a slow reaction rate. We then cultured a spheroid of HCT116 cells, which were derived from human colorectal carcinoma using a fluorescent ubiquitination-based cell cycle indicator. Fluorescence observation suggested the formation of a hypoxic and hyponutrient region within an area approximately 500 µm away from the alginate gel fiber. This indicates the development of a cancer cell aggregate culture device that enables the observation of different nutrition and oxygen states. [ABSTRACT FROM AUTHOR]

Estradiol dimers (EDs) possess significant anticancer activity by targeting tubulin dynamics. In this study, we synthesised 12 EDs variants via copper-catalysed azide-alkyne cycloaddition (CuAAC) reaction, focusing on structural modifications within the aromatic bridge connecting two estradiol moieties. In vitro testing of these EDs revealed a marked improvement in selectivity towards cancerous cells, particularly for ED1–8. The most active compounds, ED3 (IC50 = 0.38 μM in CCRF-CEM) and ED5 (IC50 = 0.71 μM in CCRF-CEM) demonstrated cytotoxic effects superior to 2-methoxyestradiol (IC50 = 1.61 μM in CCRF-CEM) and exhibited anti-angiogenic properties in an endothelial cell tube-formation model. Cell-based experiments and in vitro assays revealed that EDs interfere with mitotic spindle assembly. Additionally, we proposed an in silico model illustrating the probable binding modes of ED3 and ED5, suggesting that dimers with a simple linker and a single substituent on the aromatic central ring possess enhanced characteristics compared to more complex dimers.

Triptolide is a natural compound in herbal remedies with anti-inflammatory and anti-proliferative properties. We studied its effects on critical signaling processes within the cell, including Notch1 and STAT3 signaling. Our research showed that triptolide reduces cancer cell proliferation by decreasing the expression of downstream targets of these signals. The levels of each signal-related protein and mRNA were analyzed using Western blot and qPCR methods. Interestingly, inhibiting one signal with a single inhibitor alone did not significantly reduce cancer cell proliferation. Instead, MTT assays showed that the simultaneous inhibition of Notch1 and STAT3 signaling reduced cell proliferation. The effect of triptolide was similar to a combination treatment with inhibitors for both signals. When we conducted a study on the impact of triptolide on zebrafish larvae, we found that it inhibited muscle development and interfered with muscle cell proliferation, as evidenced by differences in the staining of myosin heavy chain and F-actin proteins in confocal fluorescence microscopy. Additionally, we noticed that inhibiting a single type of signaling did not lead to any significant muscle defects. This implies that triptolide obstructs multiple signals simultaneously, including Notch1 and STAT3, during muscle development. Chemotherapy is commonly used to treat cancer, but it may cause muscle loss due to drug-related adverse reactions or other complex mechanisms. Our study suggests that anticancer agents like triptolide, inhibiting essential signaling pathways including Notch1 and STAT3 signaling, may cause muscle atrophy through anti-proliferative activity. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSC) attract an increasing amount of attention due to their unique therapeutic properties. Yet, MSC can undergo undesirable genetic and epigenetic changes during their propagation in vitro. In this study, we investigated whether polyploidy can compromise MSC oncological safety and therapeutic properties. For this purpose, we compared the impact of polyploidy on the transcriptome of cancer cells and MSC of various origins (bone marrow, placenta, and heart). First, we identified genes that are consistently ploidy-induced or ploidy-repressed through all comparisons. Then, we selected the master regulators using the protein interaction enrichment analysis (PIEA). The obtained ploidy-related gene signatures were verified using the data gained from polyploid and diploid populations of early cardiomyocytes (CARD) originating from iPSC. The multistep bioinformatic analysis applied to the cancer cells, MSC, and CARD indicated that polyploidy plays a pivotal role in driving the cell into hypertranscription. It was evident from the upregulation of gene modules implicated in housekeeping functions, stemness, unicellularity, DNA repair, and chromatin opening by means of histone acetylation operating via DNA damage associated with the NUA4/TIP60 complex. These features were complemented by the activation of the pathways implicated in centrosome maintenance and ciliogenesis and by the impairment of the pathways related to apoptosis, the circadian clock, and immunity. Overall, our findings suggest that, although polyploidy does not induce oncologic transformation of MSC, it might compromise their therapeutic properties because of global epigenetic changes and alterations in fundamental biological processes. The obtained results can contribute to the development and implementation of approaches enhancing the therapeutic properties of MSC by removing polyploid cells from the cell population. [ABSTRACT FROM AUTHOR]

Today's advancements in technology in modern-day life have substantially raised the significance of surface plasmon resonance (SPR) sensors. In order to enhance the sensor's performance, experts are now focused on developing a SPR biomedical sensor that integrates a prism with a thin nanocomposite layer. The proposed SPR biosensor has been built with silver, BaTiO3, and 2D layering of materials (MoSe2/WS2) for the purpose to identifying skin and breast cancer cells. In this analysis, the attenuated total reflection (ATR) technique of SPR is used for the detection of skin cancer (basal cell) and breast cancer cells (MM-231 and MCF-7) to evaluate the results. It is being observed that by utilizing two metallic silver coatings with a thickness of 50 nm and 10 nm. The effectiveness of the device can be improved with two layers of WS2 (each of 0.5 nm) and two layers of BaTiO3 (each of 5 nm); the highest sensitivity can be achieved in the case of skin cancer. The numerical findings show that the basal cell's highest sensitivity is 253.5 (°/RIU) and breast (MM-231 and MCF-7) cancer cells are 309.2857°/RIU and 295.71°/RIU. The figure of merit (FoM), detection accuracy (DA), and signal-to-noise ratio (SNR) are 146.11 (RIU−1), 0.576 (degree−1), and 2.922, respectively, for basal cells, and for breast cancer, 255.66 (RIU−1), 0.829 (degree−1), and 3.59 are realized. Lastly, the numerical outcomes derived in this manuscript revealed a high degree of sensitivity and FoM compared to those of previous research studies. [ABSTRACT FROM AUTHOR]

In order to detect the cancerization of the somatic cells early, a photonic crystal fiber (PCF) sensor with double gold nanowires based on surface plasmon resonance (SPR) is designed, whose air holes are arranged periodically and symmetrically, and two gold nanowires are embedded at the outer surface of the fiber as plasma material. The performance of the sensor is numerically investigated by the finite element method (FEM). The results reveal that the proposed sensor has a high response to six types of cancerous cell detection. The spectral sensitivity and the amplitude sensitivity of MCF-7 cell can reach up to 16,357 nm/RIU and − 1242 RIU−1, respectively. The maximum resolution of the sensor for MDA-MB-231 cell is 6.11 × 10−6 RIU. In addition, the maximum spectral sensitivity of the proposed sensor is 46,800 nm/RIU in the refractive index range of 1.34 to 1.41. The proposed sensor not only can detect six cancer cells but also has potential applications in biological analysis, medical diagnosis, environmental monitoring, etc. [ABSTRACT FROM AUTHOR]

Single‐cell analysis is an emerging and promising frontier in the field of life sciences, which is expected to facilitate the exploration of fundamental laws of physiological and pathological processes. Single‐cell analysis allows experimental access to cell‐to‐cell heterogeneity to reveal the distinctive behaviors of individual cells, offering novel opportunities to dissect the complexity of severe human diseases such as cancers. Among the single‐cell analysis tools, atomic force microscopy (AFM) is a powerful and versatile one which is able to nondestructively image the fine topographies and quantitatively measure multiple mechanical properties of single living cancer cells in their native states under aqueous conditions with unprecedented spatiotemporal resolution. Over the past few decades, AFM has been widely utilized to detect the structural and mechanical behaviors of individual cancer cells during the process of tumor formation, invasion, and metastasis, yielding numerous unique insights into tumor pathogenesis from the biomechanical perspective and contributing much to the field of cancer mechanobiology. Here, the achievements of AFM‐based analysis of single cancer cells to advance physical oncology are comprehensively summarized, and challenges and future perspectives are also discussed. Research Highlights: Achievements of AFM in characterizing the structural and mechanical behaviors of single cancer cells are summarized, and future directions are discussed.AFM is not only capable of visualizing cellular fine structures, but can also measure multiple cellular mechanical properties as well as cell‐generated mechanical forces.There is still plenty of room for harnessing AFM‐based single‐cell analysis to advance physical oncology. [ABSTRACT FROM AUTHOR]

Sonodynamic therapy (SDT) is an emerging cancer treatment method in recent years. However, the ultrasound signal utilized for SDT is usually located at a low-frequency spectrum (<2 MHz), and in the field of SDT research, few studies have focused on the exploration and development of ultrasound frequency. Studies have shown that the GHz-level ultrasound can increase cell membrane permeability and have a negligible effect on cell vitality. Herein, we reported the study of a GHz thin film bulk acoustic resonator as an ultrasound source for synergistic treatment with nanoscale calcium peroxide (CaO2). It was discovered that this ultrasound source ultimately achieved an efficient therapeutic outcome on mouse breast cancer cell line 4T1. Such GHz-level ultrasound application in SDT is of high significance to broaden the cognition and application scope of SDT. [ABSTRACT FROM AUTHOR]

Gum tragacanth (GT) is a natural plant exudate discharged from the twigs and stems of Asiatic species of the Astragalus genus. GT is a heterogeneous polysaccharide which has been utilized in various biomedical fields and traditionally in ethnomedicine because of its distinctive physicochemical and biological properties, such as great biocompatibility, thermal stability biodegradability, hydrophilicity and antioxidant activity. The aim of this study was to examine whether GT has cytotoxic effects on various cancer cell lines. For this aim, four cancer cell lines i.e., human colorectal adenocarcinoma (CACO-2), glioblastoma multiforme tumor (T98G), ovarian sarcoma (SKOV-3), and breast cancer (MCF-7) cells were used. GT was prepared at the concentration of 200 µg/mL, 100 µg/mL, 50 µg/mL, 25 µg/mL and 12.5 µg/mL, using both 5% DMSO and dH2O as solvent. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) colorimetric assay was used for in vitro cytotoxicity study. GT had no cytotoxic effect on these cancer cells since cell viability percentages were found to be above 80% for all the treatments. However, remarkable dose-dependent cell proliferation efficiency of GT at certain concentrations was observed on all cancer cells except MCF-7. In conclusion, this study suggests that cancer patients should be careful about the use of GT or products containing GT due to the increasing effect of GT on the proliferation of cancer cells. [ABSTRACT FROM AUTHOR]

Fluid flow at the microscale level exhibits a unique phenomenon that can be explored to fabricate microfluidic devices integrated with components that can perform various biological functions. In this manuscript, the importance of physics for microscale fluid dynamics using microfluidic devices has been reviewed. Microfluidic devices provide new opportunities with regard to spatial and temporal control over cell growth. Furthermore, the manuscript presents an overview of cellular stimuli observed by combining surfaces that mimic the complex biochemistries and different geometries of the extracellular matrix, with microfluidic channels regulating the transport of fluids, soluble factors, etc. We have also explained the concept of mechanotransduction, which defines the relation between mechanical force and biological response. Furthermore, the manipulation of cellular microenvironments by the use of microfluidic systems has been highlighted as a useful device for basic cell biology research activities. Finally, the article focuses on highly integrated microfluidic platforms that exhibit immense potential for biomedical and pharmaceutical research as robust and portable point-of-care diagnostic devices for the assessment of clinical samples. [ABSTRACT FROM AUTHOR]

Ferrocene derivatives show a wide range of pharmacological activities in the medical field, especially in the anti‐tumor field, and can be used as candidate drugs or lead compounds for the treatment of tumors and other diseases. And α‐phenethylamine is an important intermediate for the preparation of fine chemical products. (R)‐(+)‐1‐Phenethylamine ferrocenecarboxylic acid/(S)‐(−)‐1‐phenethylamine ferrocenecarboxylic acid were prepared, named compounds 1 and 2, respectively. Single crystal X‐ray diffraction showed that compounds 1 and 2 crystallized in the orthorhombic system space group P212121, and the crystal structures of compounds 1 and 2 exhibited mirror symmetry. The inhibitory effect of two compounds on SW480, MDA‐MB‐231, and H1299 cells was tested by MTT colorimetry. The IC50 values of the compounds against cancer cells were also calculated. The anti‐cancer effect was more pronounced for compounds in the S‐configuration. Compound 2 made the wild‐type cancer cells undergo apoptosis, thus preventing cancer; it also had the function of helping the cell gene repair defects. [ABSTRACT FROM AUTHOR]

Simple Summary: We summarize the current knowledge of the signaling pathways involved in anticancer drug-induced cell death. We discuss the common signaling pathways of apoptotic cell death, antiapoptotic pathways, non-apoptotic cell death mechanisms (autophagic, necrotic, and other), signaling pathways involved in the death of drug-sensitive and -resistant tumor cells (with emphasis on c-Jun/activator protein 1 and crosstalk with mitochondrial and endoplasmic reticulum pathways), and therapeutic implications of the modification of signaling pathways leading to cell death (with emphasis on cell death-related gene targeting, interactions of drug resistance factors in drug-resistant cells, and the unfolded protein response pathway). We provide suggestions for the restoration of these altered signaling pathways to potentially restore the drug sensitivity of tumor cells. Anticancer drugs induce apoptotic and non-apoptotic cell death in various cancer types. The signaling pathways for anticancer drug-induced apoptotic cell death have been shown to differ between drug-sensitive and drug-resistant cells. In atypical multidrug-resistant leukemia cells, the c-Jun/activator protein 1 (AP-1)/p53 signaling pathway leading to apoptotic death is altered. Cancer cells treated with anticancer drugs undergo c-Jun/AP-1–mediated apoptotic death and are involved in c-Jun N-terminal kinase activation and growth arrest- and DNA damage-inducible gene 153 (Gadd153)/CCAAT/enhancer-binding protein homologous protein pathway induction, regardless of the p53 genotype. Gadd153 induction is associated with mitochondrial membrane permeabilization after anticancer drug treatment and involves a coupled endoplasmic reticulum stress response. The induction of apoptosis by anticancer drugs is mediated by the intrinsic pathway (cytochrome c, Cyt c) and subsequent activation of the caspase cascade via proapoptotic genes (e.g., Bax and Bcl-xS) and their interactions. Anticancer drug-induced apoptosis involves caspase-dependent and caspase-independent pathways and occurs via intrinsic and extrinsic pathways. The targeting of antiapoptotic genes such as Bcl-2 enhances anticancer drug efficacy. The modulation of apoptotic signaling by Bcl-xS transduction increases the sensitivity of multidrug resistance-related protein-overexpressing epidermoid carcinoma cells to anticancer drugs. The significance of autophagy in cancer therapy remains to be elucidated. In this review, we summarize current knowledge of cancer cell death-related signaling pathways and their alterations during anticancer drug treatment and discuss potential strategies to enhance treatment efficacy. [ABSTRACT FROM AUTHOR]

Identification of cancer from normal tissues is important for early diagnosis of cancer. Combined detection of multiple tumor markers is important for accurate diagnosis. It is urgent to develop fluorescent probes that are responsive to multiple cancer characterizations for selective cancer imaging. Herein, we designed a novel near‐infrared (NIR) fluorescent probe (IRAPA) using a hemi‐cyanine skeleton as fluorophore and 3‐acrylamidopropanoic ester as recognizing unit that is responsive to both oxidative and reductive molecules. IRAPA has faint fluorescence emission as the intramolecular charge transfer (ICT) process is blocked. H2O2, glutathione (GSH) and cysteine (Cys) can individually induce the hydrolysis of ester bond and give fluorescent NIR IROH. IRAPA shows low cytotoxicity and produces strong fluorescence specifically in cancer cells/tissues. While the normal cells/tissues showed very weak fluorescence. Moreover, IRAPA shows higher differences between cancer and normal cells compared to probes that only response to biothiols or ROS. [ABSTRACT FROM AUTHOR]

Sonodynamic therapy (SDT) is an emerging cancer treatment method in recent years. However, the ultrasound signal utilized for SDT is usually located at a low-frequency spectrum (<2 MHz), and in the field of SDT research, few studies have focused on the exploration and development of ultrasound frequency. Studies have shown that the GHz-level ultrasound can increase cell membrane permeability and have a negligible effect on cell vitality. Herein, we reported the study of a GHz thin film bulk acoustic resonator as an ultrasound source for synergistic treatment with nanoscale calcium peroxide (CaO2). It was discovered that this ultrasound source ultimately achieved an efficient therapeutic outcome on mouse breast cancer cell line 4T1. Such GHz-level ultrasound application in SDT is of high significance to broaden the cognition and application scope of SDT. [ABSTRACT FROM AUTHOR]

This research work introduces a Surface Plasmon Resonance (SPR) based Photonic Crystal Fiber (PCF) sensor using gold nanowires as plasmonic material designed for the detection of various cancer cells, boasting remarkable sensitivity and ease of fabrication. The sensor's structure was devised and analyzed using the Finite Element Method (FEM) of COMSOL v5.5, with a focus on exploring the impact of varying geometric parameters on its overall performance. The simulation utilized extremely fine mesh elements to ensure the utmost accuracy. Excitation between the core and plasmonic modes is achieved using Gold (Au) nanowires. The determination of the sensor's wavelength sensitivity involves assessing the resonance wavelength shift between samples of normal and cancerous cells. Simultaneously, the measurement of amplitude sensitivity is accomplished through a comparison of the amplitudes associated with their respective confinement losses. Various parameters of the PCF were varied during the experimentation, leading to the achievement of exceptionally high Amplitude Sensitivity (AS) of −273.16 RIU−1, −286.58 RIU−1, −455.59 RIU−1, −698.76 RIU−1, −1172.72 RIU−1 and −1971.30 RIU−1 for Skin Cancer, Cervical Cancer, Blood Cancer, Adrenal Gland Cancer, Breast Type-1 Cancer and Breast Type-2 Cancer respectively. Additionally, the Wavelength Sensitivity (WS) values were found to be 6500 nm/RIU, 14583.33 nm/RIU, 16428.57 nm/RIU, 25714.28 nm/RIU, 32857.14 nm/RIU, and 35714.28 nm/RIU for the same cancer types, respectively. The achieved resolutions for wavelength sensitivity are 1.54×10−5 RIU, 6.86×10−6 RIU, 6.09×10−6 RIU, 3.89×10−6 RIU, 3.04×10−6 RIU and 2.80×10−6 RIU, while the resolutions for amplitude sensitivity are 7.32×10−5 RIU, 8.37×10−5 RIU, 3.07×10−5 RIU, 2.00×10−5 RIU, 1.19×10−5 RIU and 7.10×10−6 RIU for the respective cancer types mentioned above. The design of the presented biosensor is notably uncomplicated and can be readily manufactured using contemporary fabrication techniques. In summary, the remarkable sensitivity exhibited by the proposed SPR-based PCF (SPR-PCF) biosensor, shows significant potential for enhancing the detection of cancer cells.

This research describes the methodology for synthesizing zinc oxide nanoparticles (ZnO-NPs). It demonstrates a unique, cost-effective, and non-toxic chemical technique for producing ZnO-NPs using the precipitation method with NaOH as reducing and capping agents. The formed nanoparticles have been characterized and analyzed using numerous techniques such as; Fluorescence emission spectroscopy (FL), X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy-dispersive X-ray Spectroscopy (EDX), ultraviolet–visible optical absorption (UV–Vis), Fourier transform infrared spectroscopy (FTIR), and Thermal gravimetric analysis (TGA). Also, the analytical technique X-ray diffraction studies has been used which showed that the ZnO-NPs had a Wurtzite hexagonal crystal structure with an average crystallite size of 34.27 nm. The form and the size of the synthesized ZnO-NPs have been seen in SEM and TEM photographs. Using J-image, particle size has been obtained at 13.33 nm, and the grain boundaries were all approximately spherical. Peaks in the FT-IR spectrum of the NPs indicate the presence of carboxylate (COO) and hydroxyl (O–H) functional groups. According to these findings, Zn interstitial defects are responsible for the 380 nm emission peak. Since EDX could not identify any impurities below the detection threshold, we may be sure that Zn and O are the principal components of the synthesized sample. ZnO-NPs cause an absorption band at 350.34 nm in the UV–Vis spectrum and a band gap of 3.24 eV. The catalytic activity of the synthesized ZnO nanoparticles (NPs) was evaluated by investigating their effectiveness in degrading crystal violet (CV) and methylene blue (MB) dyes, along with assessing the degradation rates. The results demonstrated a high degradation efficiency, with ZnO NPs achieving approximately 96.72 % degradation for CV and 97.169 % for MB dyes, underscoring their remarkable efficacy in the degradation process. As for antimicrobial activity assessment, the results revealed that the ZnO-NPs had negligible impact on Gram-negative bacteria, whereas they exhibited a discernible effect on Gram-positive bacteria. Additionally, it showed anti-cancer potential against colon (SW480), breast (MDA-231), and cervix (HELA) lines cells as seen by (MTT) assay. Hence, due to its simplified processes and cheaper chemicals, our synthesis technique may use in industrial settings for various applications.

Developing strategies for the radiosensitization of cancer cells by the inhibition of genes, which harbor low toxicity to normal cells, will be useful for improving cancer radiotherapy. Here, we focused on a β-site of amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1; β-secretase, memapsin-2). By functional inhibition of this peptidase by siRNA, it has also recently been shown that the DNA strand break marker, γH2AX foci, increased, suggesting its involvement in DNA damage response. To investigate this possibility, we knocked down BACE1 with siRNA in cancer cell lines, and sensitization to γ-irradiation was examined by a colony formation assay, γH2AX foci and level analysis, and flow cytometry. BACE1 knockdown resulted in the sensitization of HeLa, MDA-MB-231, U2OS, and SAOS cells to γ-irradiation in a diverse range. BACE1 knockdown showed a weak radiosensitization effect in osteosarcoma U2OS cells, which has a normal p53 function. HeLa and SAOS cells, which harbor p53 dysfunction, exhibited a greater level of radiosensitization. These results suggest that BACE1 may be a potential target for the radiosensitization in particular cancer cells.

The separation of cancer cells from blood samples is one of the most crucial tasks in cancer research. However, existing methods tend to be expensive and labor intensive. Accordingly, the present study proposes a low-cost platform that uses hydrodynamic effects for the label-free separation of cancer cells from whole blood samples using a simple centrifugal microfluidic device consisting of a Y-shaped microchannel, a contraction–expansion array (CEA) microchannel, and a bifurcation region. To enhance the separation efficiency, the input branches of the Y-shaped microchannel are designed with different widths to generate a sheath flow rate greater than the sample flow rate. As the sample flows through the CEA microchannel, the cancer cells are separated from the blood cells through inertial effects and the bifurcation law. Finally, the cancer cells are collected from the low-flow-rate branch of the bifurcation region. The feasibility of the device is first demonstrated by numerical simulations. Experimental trials are then performed to separate K562 cancer cells from blood samples with various hematocrit concentrations at disk rotational speeds ranging from 1000 to 3000 rpm. The experimental results show that the cancer cells can be successfully separated from a diluted blood sample with a ratio of 1:1.2 × 105 K562 cells to blood cells with a high efficiency of 90% at an angular velocity of 2000 rpm. [ABSTRACT FROM AUTHOR]

The present study focused on the environmentally friendly preparation, characterization, and certain biological activities of gold nanoparticles (Au-NPs) made with the Gundelia tournefortii (kenger) leaf extract. The results from devices such as transmission electron microscope, energy-dispersive x-ray spectrophotometer, and Fourier scanning electron microscope reveal the structures of nanoparticles. After an hour, the greatest surface plasmon resonance was discovered at 532.15 nm. The mean cubic crystallite size was calculated using the powder x-ray diffraction model and was found to be 23.53 nm. It was noted that the produced Au-NPs had spherical forms and hexagonal dimensions and ranged in size from 5 to 40 nm. The minimum inhibitory concentration and a colorimetric method for determining cell metabolic activity test, respectively, were used to investigate the suppressive effects of Au-NPs on the growth of pathogenic bacteria and healthy and cancer cell lines. [ABSTRACT FROM AUTHOR]

With the advancement of research on m6A-related mechanisms in recent years, the YTHDF protein family within m6A readers has garnered significant attention. Among them, YTHDF1 serves as a pivotal member, playing a crucial role in protein translation, tumor proliferation, metabolic reprogramming of various tumor cells, and immune evasion. In addition, YTHDF1 also exerts regulatory effects on tumors through multiple signaling pathways, and numerous studies have confirmed its ability to assist in the reprogramming of the tumor cell-related metabolic processes. The focus of research on YTHDF1 has shifted in recent years from its m6A-recognition and -modification function to the molecular mechanisms by which it regulates tumor progression, particularly by exploring the regulatory factors that interact with YTHDF1 upstream and downstream. In this review, we elucidate the latest signaling pathway mechanisms of YTHDF1 in various tumor cells, with a special emphasis on its distinctive characteristics in tumor cell metabolic reprogramming. Furthermore, we summarize the latest pathological and physiological processes involving YTHDF1 in tumor cells, and analyze potential therapeutic approaches that utilize YTHDF1. We believe that YTHDF1 represents a highly promising target for future tumor treatments and a novel tumor biomarker. [ABSTRACT FROM AUTHOR]

Cancer immunotherapy has emerged as a promising strategy for the treatment of cancer, with the tumor microenvironment (TME) playing a pivotal role in modulating the immune response. CD47, a cell surface protein, has been identified as a crucial regulator of the TME and a potential therapeutic target for cancer therapy. However, the precise functions and implications of CD47 in the TME during immunotherapy for cancer patients remain incompletely understood. This comprehensive review aims to provide an overview of CD47's multifaced role in TME regulation and immune evasion, elucidating its impact on various types of immunotherapy outcomes, including checkpoint inhibitors and CAR T-cell therapy. Notably, CD47-targeted therapies offer a promising avenue for improving cancer treatment outcomes, especially when combined with other immunotherapeutic approaches. The review also discusses current and potential CD47-targeted therapies being explored for cancer treatment and delves into the associated challenges and opportunities inherent in targeting CD47. Despite the demonstrated effectiveness of CD47-targeted therapies, there are potential problems, including unintended effects on healthy cells, hematological toxicities, and the development if resistance. Consequently, further research efforts are warranted to fully understand the underlying mechanisms of resistance and to optimize CD47-targeted therapies through innovative combination approaches, ultimately improving cancer treatment outcomes. Overall, this comprehensive review highlights the significance of CD47 as a promising target for cancer immunotherapy and provides valuable insight into the challenges and opportunities in developing effective CD47-targeted therapies for cancer treatment. [ABSTRACT FROM AUTHOR]

In the current study, applying simultaneously electroporation and silver nanoparticles (SNPs) are considered. Moreover, one restriction normally assigned to such nanoparticles is their side effects on the vital organs of the body. To mitigate such deleterious effects, it is better to use lower dosages of them. However, this can result in a decline in the technique's effectiveness. To compensate for the lower dose of SNPs, one can use secondary method like electroporation to deliver SNPs directly into the cells and reinforces the effect of electric pulses due to the high electrical conductivity of SNPs while having a minimal cytotoxicity effect on normal cells that are not treated with electroporation. In the present study, synergism effects of both procedures (SNPs and electroporation) experimentally and theoretically are considered to investigate the property of each technique in increasing the performance with respect to both procedures' limitations. To investigate more, adaptive neuro-fuzzy inference system (ANFIS) is used to predict the percent cell viability of cancerous cells affected by both procedures by considering amplitude and duration as inputs affecting on change of cell viability as an output. The results obtained from both experimental and simulation procedures showed that the maximum synergism between nanoparticles and electric pulses was recorded at 700 ​V/cm strength and 100 μs duration. Also, Results indicated high correlation between observed and predicted data (r2 ​= ​0.88). Moreover, the calculated root mean square error for the results of the ANFIS model was equal to 1.1. This implies that the model has practical value and can estimate the percent cell viability of cancerous cells influenced by both procedures with varying electric field amplitude and duration. This method can be proposed for other biophysical or drug delivery applications to save time and resources by utilizing the previous experimental data rather than performing more experiments.

Autophagy is a globally conserved cellular activity that plays a critical role in maintaining cellular homeostasis through the breakdown and recycling of cellular constituents. In recent years, there has been much emphasis given to its complex role in cancer stem cells (CSCs) and stem cell treatment. This study examines the molecular processes that support autophagy and how it is regulated in the context of CSCs and stem cell treatment. Although autophagy plays a dual role in the management of CSCs, affecting their removal as well as their maintenance, the intricate interaction between the several signaling channels that control cellular survival and death as part of the molecular mechanism of autophagy has not been well elucidated. Given that CSCs have a role in the development, progression, and resistance to treatment of tumors, it is imperative to comprehend their biological activities. CSCs are important for cancer biology because they also show a tissue regeneration model that helps with organoid regeneration. In other words, the manipulation of autophagy is a viable therapeutic approach in the treatment of cancer and stem cell therapy. Both synthetic and natural substances that target autophagy pathways have demonstrated promise in improving stem cell-based therapies and eliminating CSCs. Nevertheless, there are difficulties associated with the limitations of autophagy in CSC regulation, including resistance mechanisms and off-target effects. Thus, the regulation of autophagy offers a versatile strategy for focusing on CSCs and enhancing the results of stem cell therapy. Therefore, understanding the complex interactions between autophagy and CSC biology would be essential for creating therapeutic treatments that work in both regenerative medicine and cancer treatment.

In this article, Photonic crystal fiber (PCF) based surface plasmon resonance (SPR) sensor is proposed for detecting cancerous cells like Hela for cervical cancer and Basal for skin cancer. The numerical analysis and simulation of the designed biosensor is carried out using the finite element method in conjunction with a layer that is perfectly matched. The PCF sensor based on SPR has a gold layer for the plasmonic effect and a nanolayer of TiO2 to form an adhesion layer in between the gold and silica. The sensor can detect an analyte's refractive index (RI) between 1.360 and 1.392 for two distinct cancerous cell types (Hela and Basal). The proposed biosensor's performance is evaluated using amplitude and wavelength investigation techniques. This study achieves the wavelength sensitivity of 6250 nm/RIU, 5000 nm/RIU, and the amplitude sensitivity of 909.05 RIU−1, 505.53 RIU−1 for Hela and Basal cells, respectively. The results show that the proposed sensor is suitable for real-time biosensing applications.

This study presents the design and numerical analysis of an optical biosensor utilizing a photonic crystal resonator to detect alterations in the refractive index in human blood. The biosensor has potential applications for early diagnosis of cancer cells and various viruses. The structure of the biosensor being proposed is comprised of a waveguide and an oval ring resonator, designed via silicon rods in a 2D square lattice. Accurate detection can lead to choosing the best therapeutic approach and accelerate the patient’s recovery, which is possible by utilizing this biosensor. An optimized and compact design of biosensor (10.2 μm × 7.5 μm) with a significant detection resolution and detection limit of 1∗10-4 , a wide range of cell and virus detection from a refractive index of (1.330 ∼ 1.401) proposed to be implemented in real-time medical applications The proposed sensor has a good figure of merit, and high sensitivity values ranging between 650 and 900. Accordingly, an improved sensor with a quality factor as high as 190 is achieved. Through the implementation of the finite-difference time-domain (FDTD) method, the resonator's reaction to perturbations induced by cells and viruses present in the blood is investigated. The exceptional characteristics of biosensor make it one of the potential candidates in the field of biomedical sensing, which exhibits better sensitivity at the Terahertz band, compared to prior works.

Resistance to chemo- or radiotherapy is the main obstacle to consistent treatment outcomes in oncology patients. A deeper understanding of the mechanisms driving the development of resistance is required. This review focuses on secretory factors derived from chemo- and radioresistant cancer cells, cancer-associated fibroblasts (CAFs), mesenchymal stem cells (MSCs), and cancer stem cells (CSCs) that mediate the development of resistance in unexposed cells. The first line of evidence considers the experiments with conditioned media (CM) from chemo- and radioresistant cells, CAFs, MSCs, and CSCs that elevate resistance upon the ionizing radiation or anti-cancer drug exposure of previously untreated cells. The composition of CM revealed factors such as circular RNAs; interleukins; plasminogen activator inhibitor; and oncosome-shuttled lncRNAs, mRNAs, and miRNAs that aid in cellular communication and transmit signals inducing the chemo- and radioresistance of sensitive cancer cells. Data, demonstrating that radioresistant cancer cells become resistant to anti-neoplastic drug exposure and vice versa, are also discussed. The mechanisms driving the development of cross-resistance between chemotherapy and radiotherapy are highlighted. The secretion of resistance-mediating factors to intercellular fluid and blood brings attention to its diagnostic potential. Highly stable serum miRNA candidates were proposed by several studies as prognostic markers of radioresistance; however, clinical studies are needed to validate their utility. The ability to predict a treatment response with the help of the miRNA resistance status database will help with the selection of an effective therapeutic strategy. The possibility of miRNA-based therapy is currently being investigated with ongoing clinical studies, and such approaches can be used to alleviate resistance in oncology patients. [ABSTRACT FROM AUTHOR]

In preparing space and microgravity experiments, the utilization of ground-based facilities is common for initial experiments and feasibility studies. One approach to simulating microgravity conditions on Earth is to employ a random positioning machine (RPM) as a rotary bioreactor. Combined with a suitable low-mass model system, such as cell cultures, these devices simulating microgravity have been shown to produce results similar to those obtained in a space experiment under real microgravity conditions. One of these effects observed under real and simulated microgravity is the formation of spheroids from 2D adherent cancer cell cultures. Since real microgravity cannot be generated in a laboratory on Earth, we aimed to determine which forces lead to the detachment of individual FTC-133 thyroid cancer cells and the formation of tumor spheroids during culture with exposure to random positioning modes. To this end, we subdivided the RPM motion into different static and dynamic orientations of cell culture flasks. We focused on the molecular activation of the mechanosignaling pathways previously associated with spheroid formation in microgravity. Our results suggest that RPM-induced spheroid formation is a two-step process. First, the cells need to be detached, induced by the cell culture flask's rotation and the subsequent fluid flow, as well as the presence of air bubbles. Once the cells are detached and in suspension, random positioning prevents sedimentation, allowing 3D aggregates to form. In a comparative shear stress experiment using defined fluid flow paradigms, transcriptional responses were triggered comparable to exposure of FTC-133 cells to the RPM. In summary, the RPM serves as a simulator of microgravity by randomizing the impact of Earth's gravity vector especially for suspension (i.e., detached) cells. Simultaneously, it simulates physiological shear forces on the adherent cell layer. The RPM thus offers a unique combination of environmental conditions for in vitro cancer research. [ABSTRACT FROM AUTHOR]

The biophysical properties of cells described at the level of whole cells or their membranes have many consequences for their biological behavior. However, our understanding of the relationships between mechanical parameters at the level of cell (stiffness, viscoelasticity) and at the level of the plasma membrane (fluidity) remains quite limited, especially in the context of pathologies, such as cancer. Here, we investigated the correlations between cells' stiffness and viscoelastic parameters, mainly determined via the actin cortex, and plasma membrane microviscosity, mainly determined via its lipid profile, in cancer cells, as these are the keys to their migratory capacity. The mechanical properties of cells were assessed using atomic force microscopy (AFM). The microviscosity of membranes was visualized using fluorescence-lifetime imaging microscopy (FLIM) with the viscosity-sensitive probe BODIPY 2. Measurements were performed for five human colorectal cancer cell lines that have different migratory activity (HT29, Caco-2, HCT116, SW 837, and SW 480) and their chemoresistant counterparts. The actin cytoskeleton and the membrane lipid composition were also analyzed to verify the results. The cell stiffness (Young's modulus), measured via AFM, correlated well (Pearson r = 0.93) with membrane microviscosity, measured via FLIM, and both metrics were elevated in more motile cells. The associations between stiffness and microviscosity were preserved upon acquisition of chemoresistance to one of two chemotherapeutic drugs. These data clearly indicate that mechanical parameters, determined by two different cellular structures, are interconnected in cells and play a role in their intrinsic migratory potential. [ABSTRACT FROM AUTHOR]