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Supramolecular chemistry has garnered important interest in recent years toward improving therapeutic efficacy via drug delivery approaches. Although self-assemblies have been deeply investigated, the design of novel drugs leveraging supramolecular chemistry is less known. In this contribution, we show that a Low Molecular Weight Gel (LMWG) can elicit cancer cell apoptosis. This biological effect results from the unique supramolecular properties of a bolaamphiphile-based gelator, which allow for strong interaction with the lipid membrane. This novel supramolecular-drug paradigm opens up new possibilities for therapeutic applications targeting membrane lipids.

PS-B1 は、ヒト常在乳酸菌21種を大豆粉培地を主栄養源とし共棲培養して得られた培養ろ液で、乳酸菌群が生産した種々の代謝物質を含む、いわゆる、バイオジェニックスに位置づけられるものである。我々は、PS-B1 の有効生理活性について多方面から研究し、PS-B1 の健康保全・疾病予防を指向したバイオジェニックスフードとしての可能性を評価するためにエビデンスを蓄積してきた。本稿では、PS-B1 の有効生理活性の解析結果として、PS-B1 のがん細胞株増殖抑制作用、肝保全作用、および肥満抑制と脂質代謝改善作用について述べる。

Background Dysregulated endothelial cell growth is involved in many types of human cancer, including cervical cancer. LncRNA GATA6-AS was reported to regulate endothelial cell growth, suggesting it might involve in cervical cancer. Our study was carried out to explore the involvement of GATA6-AS in cervical squamous cell carcinoma (CSCC), a subtype of cervical cancer. Methods To explore the expression of GATA6-AS, RT-qPCR was performed to detect GATA6-AS in plasma of 65 CSCC patients and 58 healthy females. To detect the expression of GATA6-AS, total RNAs were extracted. Results We found that plasma GATA6-AS expression was down-regulated in CSCC patients than that in healthy females, and HPV infection did not significantly affect the plasma expression of GATA6-AS. Moreover, we found that plasma GATA6-AS showed diagnostic values for CSCC by performing ROC curve analysis. The expression of miR-205 in plasma was also found to be up-regulated in CSCC patients than that in healthy females and inversely correlated with the expression of GATA6-AS in CSCC patients. Furthermore, over-expression of miR-205 did not significantly affect the expression of GATA6-AS in CSCC cells, while over-expression of GATA6-AS down-regulated miR-205 expression. In addition, GATA6-AS over-expression inhibited CSCC cell proliferation and promoted CSCC cell apoptosis, while miR-205 over-expression played opposite roles and attenuated the effects of GATA6-AS over-expression on CSCC cells. Conclusion Taken together, these results suggest that GATA6-AS may inhibit cell proliferation and promote cell apoptosis in CSCC by down-regulating miR-205.

Camptothecin (CPT) and its analogues show potent antitumour activity. However, poor water solubility and severe side effects have restricted their applications in clinical practice. In this paper, a novel self-assembly based on camptothecin and carbamoylmannose conjugates (CPT-Man) was constructed. The self-assembly increased the water solubility of camptothecin to 0.64 mg/ml and antitumour activity. Moreover, CPT-Man could induce obvious cancer cell apoptosis. This work provides a new approach for exploring carbohydrate-modified antitumour properties by self-assembled CPT drugs.

The detailed mechanism and the extent of pH/SO2 changes during apoptosis remain unknown. The developed sensor NPCF for SO2 and pH dual detection illustrates that SO2 can reduce the inflammation caused by LPS and the acidification of the environment. The levels of SO2 and pH change during carbonyl cyanide m-chlorophenylhydrazone (CCCP)-induced apoptosis.

c-Jun N-terminal kinase (JNK) signalling regulates both cancer cell apoptosis and survival. Emerging evidence show that JNK promoted tumour progression is involved in various cancers, that include human pancreatic-, lung-, and breast cancer. The pro-survival JNK oncoprotein functions in a cell context- and cell type-specific manner to affect signal pathways that modulate tumour initiation, proliferation, and migration. JNK is therefore considered a potential oncogenic target for cancer therapy. Currently, designing effective and specific JNK inhibitors is an active area in the cancer treatment. Some ATP-competitive inhibitors of JNK, such as SP600125 and AS601245, are widely used in vitro; however, this type of inhibitor lacks specificity as they indiscriminately inhibit phosphorylation of all JNK substrates. Moreover, JNK has at least three isoforms with different functions in cancer development and identifying specific selective inhibitors is crucial for the development of targeted therapy in cancer. Some selective inhibitors of JNK are identified; however, their clinical studies in cancer are relatively less conducted. In this review, we first summarised the function of JNK signalling in cancer progression; there is a focus on the discussion of the novel selective JNK inhibitors as potential targeting therapy in cancer. Finally, we have offered a future perspective of the selective JNK inhibitors in the context of cancer therapies. We hope this review will help to further understand the role of JNK in cancer progression and provide insight into the design of novel selective JNK inhibitors in cancer treatment.

The number of death due to cancer-related diseases each year is at the alarming level and is constantly growing. Tools that can effectively and conveniently detect cancer cell apoptosis can play a significant role in cancer research, cancer therapy, and other related industries. Herein, we fabricated, for the first time, an ultrasensitive, disposable, self-enhanced off-on electrochemiluminescence (ECL) biosensor based on ternary Ru-PEI@PCN-333(Al) system to determine caspase-3 activity, the biomarker of apoptosis. The biosensor had a low detection limit of 0.017 pg/mL and was able to enhance the ECL emission and stability. A solid-state (SS) ECL strategy was adopted to overcome the relatively weak ECL emission due to the long distance between electrochemiluminophore and electrode surface. The analysis requires only one incubation step, which can significantly reduce the operational complexity and time. The biosensor had higher sensitivity, and the off-on ECL mode was achieved using caspase-3 as a switch. The on-site and rapid detection capability of the biosensor was achieved by the introduction of disposable screen-printed electrodes (SPEs). This study lays a foundation for the development of more advanced, ingenious, portable and reliable ECL devices for biosensing not only caspase-3, but also other bioanalytes.

This study aimed to detect miR-455-5p and S1PR1 proteins using nanoparticle-assisted polymerase chain reaction (nano-PCR) to determine their correlation with cervical carcinoma prognosis. To achieve this study’s goals, we selected 48 cervical carcinoma patients between January 2014 to January 2016 and subjected them to the miR-455-5p test by nano-PCR. The collected samples were then divided into two groups based on miR-455-5p levels. We had four HeLa cell groups, one group as the control, and one group overexpressed the miR-455-5p protein. A third group was miR-455-5p silent, and a separate group overexpressed both the miR-455-5p and S1PR1 proteins. Results also proved that the nano-PCR had a higher sensitivity than RT-PCR, and patients with poor prognosis had lesser miR-455-5p levels. Similarly, high levels of miR-455-5 contributed to cancer cell apoptosis and migration inhibition by targeting S1PR1 expression negatively. These two biomarkers are therefore significantly related to the prognosis of cervical carcinoma patients.

Chaetocin is a natural metabolite product with various biological activities and pharmacological functions isolated from Chaetomium species fungi belonging to the thiodiketopyrazines. Numerous studies have demonstrated a wide range of antitumor activities of chaetocin in vitro and in vivo. Several studies have demonstrated that chaetocin suppresses the growth and proliferation of various tumour cells by regulating multiple signalling pathways related to tumour initiation and progression, inducing cancer cell apoptosis (intrinsic and extrinsic), enhancing autophagy, inducing cell cycle arrest, and inhibiting tumour angiogenesis, invasion, and migration. The antitumor effects and molecular mechanisms of chaetocin are reviewed and analysed in this paper, and the prospective applications of chaetocin in cancer prevention and therapy are also discussed. This review aimed to summarize the recent advances in the antitumor activity of chaetocin and to provide a rationale for further exploring the potential application of chaetocin in overcoming cancer in the future.

Erianin is the major bisbenzyl compound extracted from the traditional Chinese medicine Dendrohium chrysotoxum Lindl. Erianin possesses many biological properties relevant to cancer prevention and therapy. The previous studies confirmed that antitumor effects of erianin are regulated with multiple signaling pathways. The mechanisms of erianin are numerous, and most of them induce cancer cell apoptosis that may be intrinsic or extrinsic and modulate the ROS/JNK signaling pathways. Invasion, migration, and angiogenesis represent emerging targets of erianin and support its anticancer properties. This review aimed to summarize the recent advances in the antitumor activity of erianin and to provide a rationale for further exploring the potential application of erianin in overcoming cancer in the future.

We report here the synthesis, characterization of seventeen (E)-2-methyl-3-ferrocenyl-N-acrylamides. The single crystal structures of the key intermediate b and two target compounds d5 and d6 were confirmed by X-ray crystallographic analysis. Antitumor activity of all compounds was tested in vitro. Compound d1 was the most significant one against B16 F10 cell line, indicating that it could be a good candidate for further study. Furthermore, cancer cell apoptosis assay was performed and the result indicated that compound d1 effectively fueled B16 F10 cells apoptosis in a dose-dependent manner.

GPR55 is a GPCR of the non-CB1/CB2 cannabinoid receptor family, which is activated by lysophosphatidylinositol (LPI) and stimulates the proliferation of cancer cells. Anandamide, a bioactive lipid endocannabinoid, acts as a biased agonist of GPR55 and induces cancer cell death, but is unstable and psychoactive. We hypothesized that other endocannabinoids and structurally similar compounds, which are more hydrolytically stable, could also induce cancer cell death via GPR55 activation. We chemically synthesized and tested a set of fatty acid amides and esters for cell death induction via GPR55 activation. The most active compounds appeared to be N-acyl dopamines, especially N-docosahexaenoyl dopamine (DHA-DA). Using a panel of cancer cell lines and a set of receptor and intracellular signal transduction machinery inhibitors together with cell viability, Ca2+, NO, ROS (reactive oxygen species) and gene expression measurement, we showed for the first time that for these compounds, the mechanism of cell death induction differed from that published for anandamide and included neuronal nitric oxide synthase (nNOS) overstimulation with concomitant oxidative stress induction. The combination of DHA-DA with LPI, which normally stimulates cancer proliferation and is increased in cancer setting, had an increased cytotoxicity for the cancer cells indicating a therapeutic potential.

Regular physical activity reduces the risk of several site-specific cancers in humans and suppresses tumour growth in animal models. The mechanisms through which exercise reduces tumour growth remain incompletely understood, but an intriguing and accumulating body of evidence suggests that the incubation of cancer cells with post-exercise serum can have powerful effects on key hallmarks of cancer cell behaviour in vitro. This suggests that exercise can impact tumour biology through direct changes in circulating proteins, RNA molecules and metabolites. Here, we provide a comprehensive narrative overview of what is known about the effects of exercise-conditioned sera on in vitro cancer cell behaviour. In doing so, we consider the key limitations of the current body of literature, both from the perspective of exercise physiology and cancer biology, and we discuss the potential in vivo physiological relevance of these findings. We propose key opportunities for future research in an area that has the potential to identify key anti-oncogenic protein targets and optimise physical activity recommendations for cancer prevention, treatment and survivorship.

Highlights • Voltage-gated potassium channels Kv1.3 are important in normal and cancer tissues. • Inhibition of the channels may find application in therapy of some cancer disorders. • Simvastatin, mevastatin and pravastatin inhibit Kv1.3 channels in cancer cells. • The strongest channel inhibitor is simvastatin and the weakest is pravastatin. • The channel inhibition may be involved in anti-cancer activity of the statins., Voltage-gated potassium channels are integral membrane proteins selectively permeable for potassium ions and activated upon change of membrane potential. Voltage-gated potassium channels of the Kv1.3 type were discovered both in plasma membrane and in inner mitochondrial membrane (mito Kv1.3 channels). For some time Kv1.3 channels located both in plasma membrane and in mitochondria are considered as a potentially new molecular target in several pathologies including some cancer disorders. Lipophilic nontoxic organic inhibitors of Kv1.3 channels may potentially find a clinical application to support therapy of some cancer diseases such as breast, pancreas and lung cancer, melanoma or chronic lymphocytic leukaemia (B-CLL). Inhibition of T lymphocyte Kv1.3 channels may be also important in treatment of chronic and acute respiratory diseases including severe pulmonary complication in corona virus disease Covid 19, however further studies are needed to confirm this supposition. Statins are small-molecule organic compounds, which are lipophilic and are widely used in treatment of hypercholesterolemia and atherosclerosis. Electrophysiological studies performed in our laboratory showed that statins: pravastatin, mevastatin and simvastatin are effective inhibitors of Kv1.3 channels in cancer cells of human T cell line Jurkat. We showed that application of the statins in the concentration range from 1.5 μM to 50 μM inhibited the channels in a concentration-dependent manner. The inhibitory effect was the most potent in case of simvastatin and the least potent in case of pravastatin. The inhibition was partially irreversible in case of simvastatin and fully reversible in case of pravastatin and mevastatin. It was accompanied by a significant acceleration of the current inactivation rate without any significant change of the activation rate. Mechanism of the inhibition is probably complex, including a direct interaction with the channel protein and perturbation of lipid bilayer structure, leading to stabilization of the inactivated state of the channels., Graphical abstract Image, graphical abstract

We made a big breakthrough in nanomaterial-based cancer therapy by developing nanomaterials consisting of tellurium and selenium., Two-dimensional nanomaterial-based photothermal therapy (PTT) is currently under intensive investigation as a promising approach toward curative cancer treatment. However, high toxicity, moderate efficacy, and low uniformity in shape remain critical unresolved issues that hamper their clinical application. Thus, there is an urgent need for developing versatile nanomaterials to meet clinical expectations. To achieve this goal, we developed a stable, highly uniform in size, and nontoxic nanomaterials made of tellurium-selenium (TeSe)–based lateral heterojunction. Systemic delivery of TeSe nanoparticles in mice showed highly specific accumulation in tumors relative to other healthy tissues. Upon exposure to light, TeSe nanoparticles nearly completely eradicated lung cancer and hepatocellular carcinoma in preclinical models. Consistent with tumor suppression, PTT altered the tumor microenvironment and induced immense cancer cell apoptosis. Together, our findings demonstrate an exciting and promising PTT-based approach for cancer eradication.

Sepiapterin reductase plays an enzymatic role in the biosynthesis of tetrahydrobiopterin, which is reported in limited studies to regulate the progression of several tumors. However, the role of sepiapterin reductase in hepatocellular carcinoma remains largely unknown. Here, we found that sepiapterin reductase was frequently highly expressed in human hepatocellular carcinoma, which was significantly associated with higher T stage, higher tumor node metastasis stage, and even shorter survival of hepatocellular carcinoma patients. Furthermore, cell and animal experiments showed that sepiapterin reductase depletion inhibited cancer cell proliferation and promoted cancer cell apoptosis. Importantly, the results suggested that sepiapterin reductase enzymatic activity was not necessary for the progression of hepatocellular carcinoma, based on the comparison between SMMC-7721 and SMMC-7721 containing sepiapterin reductase mutant. Moreover, we showed that sepiapterin reductase regulated the development of hepatocellular carcinoma via the FoxO3a/Bim-signaling pathway. Collectively, our study suggests that sepiapterin reductase controls hepatocellular carcinoma progression via FoxO3a/Bim signaling in a nonenzymatic manner, which provides a potential prognostic factor and therapeutic strategy for hepatocellular carcinoma.

Telmisartan (TMST) can block selectively and irreversibly an angiotensin II receptor type 1 (AT1), but has no effect on other receptor systems and also induce human prostate cancer cell apoptosis. In this work, domain specific association of TMST with calf thymus DNA was explored through multi-spectral methodologies and theoretical calculation. The results of absorption spectroscopy revealed that TMST interacting with ct-DNA formed the TMST–ct-DNA complex through non-covalent interaction and the association constant (Ka) was of 2.71 × 103 M−1 at 298 K. Based on the thermodynamic analysis, it can be inferred that the interacting TMST with ct-DNA was an enthalpy-driven, spontaneous, and exothermic process due to the ΔG0 T|ΔS0| under the studied temperature ranges. The domain interacting forces for interacting TMST with ct-DNA were van der Waals forces and hydrogen bonding interaction due to the ΔH0

Background Apoptosis is one of the pathways of programmed cell death (PCD), which leads to pathognomic cellular changes different from cellular necrosis. It includes the death receptor pathway and the mitochondrial pathway, both of which involve many key proteins abnormally expressed in apoptosis-related diseases, such as cancer. The majority of anti-cancer natural products promote apoptosis to induce cancer cell death. In this review, we aim to survey the current knowledge on key apoptotic proteins and some representative natural products that can induce cancer cell apoptosis by regulating these proteins. Method We reviewed the recent relative literatures using a structured search of bibliographic databases, and the keywords, such as natural products, cancer therapy, and apoptosis pathway, were used for inclusion/exclusion criteria. Results One hundred and seventy-one papers are included in this review. Numerous natural products have been reported to induce cell apoptosis by regulating the expression of key apoptotic proteins, leading to a variety of antitumor effects. This review identifies the major apoptotic proteins and elaborates the interaction between the apoptotic proteins and various natural anti-cancer products. Conclusion This review provides substantial evidences of apoptosis pathways in cancer cells and the apoptotic proteins modulated by active natural products, which may help to gain a comprehensive understanding for the development of natural drugs for better cancer treatment.

Moringa oleifera is widely cultivated as an important vegetable for human consumption. Moringa contains numerous dietary phytonutrients, including flavonoids, which are secondary plant metabolites with health-promoting effects, such as prevention of damage to normal cell DNA and promotion of cancer cell apoptosis, thereby reducing the burden of non-communicable diseases (NCDs). Therefore, flavonoids in M. oleifera have attracted great interest as chemotherapeutic modality due to its edible, potential anti-inflammatory, antioxidant and larger amounts of flavonoids compared with other vegetables and fruit. This review focuses on the findings of current studies of the health-promoting aspects of Moringa and Moringa extract-related flavonoids on NCDs, particularly cancer, diabetes and obesity. According to the available literature, the beneficial effects of bioactive flavonoids in M. oleifera as a future medicinal food are promising but further evidence from human studies, including clinical trials, is required.

Aim: Using cytotoxic agents with apoptosis induction may represent one of new strategies for cancer treatment to overcome the increased resistance of the disease. Methodology: Two series of benzo[f][1,4]oxazepine-3,5(2H,4H)-diones (compounds 5, 6a–f) and 3-phenylbenzo[f][1,4]oxazepin-5(4H)-ones (compounds 10, 11a-f) were synthesized and screened for their cytotoxicity against leukemia K-562 and breast T-47D cancer cell lines as well as normal fibroblasts WI-38. Results: The tested compounds revealed good cytotoxicity and selectivity toward cancer cell lines relative to the normal cells, especially compounds 6f, 10 and 11e, f. These compounds were screened for cell cycle disturbance and apoptosis induction. They were found to cause PreG1 apoptosis and complete cell growth arrest at G2/M. They induce apoptosis via caspase-3 and Bax activation and downregulation of Bcl2. Conclusion: benzo[f][1,4]oxazepine represents a scaffold for further optimization to obtain promising anticancer agents.

Lysosomal micropolarity-change is one of the ultimate reflection factors of cell apoptosis and death in complex living organism. Thus, rapid and sensitive detecting of lysosomal micropolarity-change is beneficial for real-time estimating of cancer cell apoptosis. Many polarity-specific fluorescent probes have been reported, but lysosomal micropolarity-ultrasensitive ratiometric fluorescent probe with excellent two-photon property for real-time estimating the cancer cell apoptosis is scarce. In this work, an intramolecular charge transfer (ICT) two-photon ratiometric fluorescent probe (DC) was reported and evaluated to real-time estimate cancer cell apoptosis through ultrasensitive detection of lysosomal micro-polarity. DC appeared different fluorescence intensities at 580 and 600 nm in cancer cells, specifically. And its fluorescence change presented a linear change on ratio mode in the range of polarity (Δf = 0.2230–0.3274). The lowest detection of DC for polarity change can as low as Δf = 0.018 by fluorescent ratiometric signals. More importantly, based on the ultrasensitive changes of lysosomal micro-polarity, DC can be used to real-time estimate cancer cell apoptosis by microscopic imaging and flow cytometry. Thus, DC may have potential application varying from detecting of lysosomal micropolarity changes to real-time estimating of cancer cell apoptosis.

Sea cucumber is marine biota with a high economic value and also has potential for anti-cancer. The purpose of this study was to explore the mechanism of active compound of Bohadschia argus on regulating cancer cell survival. The B. argus samples were collected from the sea of Kamal Village, West Seram Maluku, then extracted by water. The constituents of water extract of B. argus were examined by LC-MS. The network among active compound and its protein target were determined by Cytoscape app. The result shows that B. argus has several active compounds, such as chondroitin sulfate, holothurin A, holothurin B, and scabraside that might play a role in cancer cell apoptosis, proliferation, and metastasis. Keywords: Active compound , Bohadschia argus , LC-MS.

Tetraiodothyroaetic acid (tetrac) is a derivative of L-thyroxine with anticancer properties. By multiple molecular mechanisms, tetrac and chemically-modified tetrac induce apoptosis in a variety of human cancer cells in vitro and in xenografts. The anticancer activities of tetrac are initiated at the thyroid hormone analogue receptor on the extracellular domain of plasma membrane integrin αvβ3 (PJ Davis et al., Physiol Rev 101:319-352, 2021). Induction of apoptosis in glioblastoma xenograft with chemically modified tetrac (P-bi-TAT) has yielded 90% in volume of grafts that continues after discontinuation of tetrac. In the present study, we show that human glioblastoma xenograft shrinkage in response to P-bi-TAT is associated with local appearance of phagocytic monocytes and clearance of apoptotic debris (efferocytosis). Primary culture xenograft of glioblastoma cells (GBM 052814, kindly provided by the University of Pittsburgh Medical Center, Department of Neurosurgery) and U87-luc (ATCC, Manassas, VA) xenografts were generated in 5-member groups of nude mice for each tumor cell type and for controls. Five days post-implantation, injection of animals was begun with PBS (control) or P-bi-TAT (10 mg/kg body weight). Injection was continued X21 days and animals were then maintained off-treatment for an additional 21 days. Tumors were harvested, formalin-fixed and slide-mounted, then analyzed by TUNEL assay for apoptosis and by anti-CD68 staining for monocytic macrophage content. Histologic analysis (H&E staining) was also carried out. TUNEL analysis and histopathology of both xenograft models revealed more than 90% apoptotic change with 21-days of P-bi-TAT treatment (P

Selecting the available treatment for each cancer patient from genomic context is a core goal of precision medicine, but innovative approaches with mechanism interpretation and improved performance are still highly needed. Through utilizing in vitro chemotherapy response data coupled with gene and miRNA expression profiles, we applied a network-based approach that identified markers not as individual molecules but as functional groups extracted from the integrated transcription factor and miRNA regulatory network. Based on the identified chemoresponse communities, the predictors of drug resistance achieved high accuracy in cross-validation and were more robust and reproducible than conventional single-molecule markers. Meanwhile, as candidate communities not only enriched abundant cellular process but also covered a variety of drug enzymes, transporters, and targets, these resulting chemoresponse communities furnished novel models to interpret multiple kinds of potential regulatory mechanism, such as dysregulation of cancer cell apoptosis or disturbance of drug metabolism. Moreover, compounds were linked based on the enrichment of their common chemoresponse communities to uncover undetected response patterns and possible multidrug resistance phenotype. Finally, an omnibus repository named ChemoCommunity (http://www.jianglab.cn/ChemoCommunity/) was constructed, which furnished a user-friendly interface for a convenient retrieval of the detailed information on chemoresponse communities. Taken together, our method, and the accompanying database, improved the performance of classifiers for drug resistance and provided novel model to uncover the possible regulatory mechanism of individual response to drug.

Starting from two ferrocene-based pyrimidinamines (3 and 8), two series of novel ferrocene bisamide derivatives (4a-m and 9a-m) were synthesized and characterized, respectively. Both 3 and 8 gave single crystals suitable for X-ray structural analysis. All the corresponding bisamide derivatives were evaluated the inhibitory activities against B16-F10 and A549 cell lines using the MTT method. Among them, compound 4d exhibited comparable antitumor activities in vitro against B16-F10 and compound 9d exhibited significant antitumor activities in vitro against A549. Cancer cell apoptosis assay were performed and results indicated that compound 9d effectively fuels A549 cells apoptosis in a dose-dependent manner.

Nitric oxide (NO) has recently joined the clinical arena of cancer therapy because high levels of NO could not only induce cytotoxicity and apoptosis of cancer cells, but also sensitize the cells to chemo- and radio-therapies. Diazeniumdiolates are an important class of NO donors, and the O2-alkylation, arylation and sulfonylation of diazeniumdiolates result in more stable and potent anticancer agents. However, O2-phosphorylation has so far not been reported yet. Herein, we describe the design, synthesis and biological evaluation of a group of phosphorodiamidate mustard-based O2-phosphorylated diazeniumdiolates, 6–9. The most active compound, 7, was comparable, or even more potent, than a known anticancer agent, O2-2,4-dinitrobenzene diazeniumdiolate JS-K, against six cancer cell lines. Furthermore, 7 released larger amounts of NO, caused more significant DNA damage and cancer cell apoptosis than JS-K in the cancer cells. Our findings suggest that this new type of O2-substituted diazeniumdiolate could be potentially applied in the fight against cancer.

Background: In spite of the advances in Cancer treatment, limitations exist. Refractory cases and late presentations are particularly worrying. The uncertainty of cure and the high costs have led to the popularly of complementary and alternative medicine in cancer treatment. Herbal medicine has particular attraction because it has been shown to be working on a multi-targets direction: promoting apoptosis of cancer cells, anti-angiogenesis and immunomodulating. Research on creating a simple herbal formula with multiple effects of cancer control has started and showed in laboratory platforms promising results. Metronomic Chemotherapy: Attention on the use of old oral cytotoxic drugs in small doses for refractory and late cancer cases has started more than a decade. Satisfactory and good results have been found to be related to anti-angiogenesis, immunomodulations and cancer cell apoptosis. These findings are comparable to the use of multiple targets herbal medicine. Conclusion: Assumption is made that metronomic chemotherapy, combined with herbal medicine could be achieving synergistic effects and would be affordable to all patients.

A series of new allylated mono-carbonyl curcumin analogues (MACs) were designed and synthesized. In vitro cytotoxic activities of allylated MACs 6a-h together with previously reported analogues 4a-i and 7a-e, were tested against human cholangiocarcinoma cell lines including HUCCA, QBC-939 and RBE. Of all the compounds tested, 6c exhibited potent in vitro antiproliferative activity against the three tested cancer cell lines with IC50 values of 8.7, 9.3 and 8.9μM, respectively. Cell cycle analysis showed that 6c inhibited cell proliferation due to G2/M arrest. Furthermore, mechanistic studies revealed that 6c dose-dependently increased the level of Bax and inhibited the expression of Bcl-2, to induce cancer cell apoptosis. Taken together, this work provides a novel series of anti-cancer candidates for the treatment of cholangiocarcinoma.

A unique model of a Metasurface that works as a biosensor to distinguish carcinoma cells on Terahertz time domain spectroscopy has been designed exploiting metamaterials. Cancer cell apoptosis by the action of drug concentration is monitored using the resonating frequency shift of the double split ring resonator inculcating double asymmetry. The structure that controls the plasma response of the metamaterial is explicitly made to degrade after the completion of medication.