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Abstract Traditional Chinese medicine (TCM) is considered to be one of the most comprehensive and influential form of traditional medicine. It plays an important role in clinical treatment and adjuvant therapy for cancer. However, the complex composition of TCM presents challenges to the comprehensive and systematic understanding of its antitumor mechanisms, which hinders further development of TCM with antitumor effects. Omics technologies can immensely help in elucidating the mechanism of action of drugs. They utilize high-throughput sequencing and detection techniques to provide deeper insights into biological systems, revealing the intricate mechanisms through which TCM combats tumors. Multi-omics approaches can be used to elucidate the interrelationships among different omics layers by integrating data from various omics disciplines. By analyzing a large amount of data, these approaches further unravel the complex network of mechanisms underlying the antitumor effects of TCM and explain the mutual regulations across different molecular levels. In this study, we presented a comprehensive overview of the recent progress in single-omics and multi-omics research focused on elucidating the mechanisms underlying the antitumor effects of TCM. We discussed the significance of omics technologies in advancing research on the antitumor properties of TCM and also provided novel research perspectives and methodologies for further advancing this research field.

Abstract Breast cancer (BC) remains a significant health concern for women globally, prompting the relentless pursuit of novel therapeutic modalities. As a traditional Chinese medicine, Boswellia carterii has been extensively used to treat various cancers, such as BC. However, the anti-BC effect and underlying mechanism of Boswellia carterii remain largely unclear. The aim of this study is to explore the therapeutic effect of Boswellia carterii n-hexane extract (BCHE) against BC as well as its underlying mechanism. The present study showed that BCHE significantly suppressed the viability of human BC cells. Moreover, BCHE exhibited potent anti-BC activity in vivo with no significant toxic effects. Additionally, BCHE induced ferroptosis via increased Transferrin expression and the intracellular accumulation of Fe2+, as well as decreased glutathione peroxidase 4 (GPX4) expression and the upregulation of reactive oxygen species (ROS)-induced lipid peroxidation in BC cells. In vivo experimental results also demonstrated that BCHE effectively induced ferroptosis through GPX4 downregulation and Transferrin upregulation in tumor-bearing mice. Overall, BCHE inhibited the growth of BC cells by inducing ferroptosis mediated by modulating the iron accumulation pathway and the lipid peroxidation pathway. Therefore, BCHE could serve as a potential ferroptosis-targeting drug for treating BC.

Abstract Background The dysregulated mechanistic target of rapamycin complex 1 (mTORC1) signaling plays a critical role in ferroptosis resistance and tumorigenesis. However, the precise underlying mechanisms still need to be fully understood. Methods Endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) expression in mTORC1-activated mouse embryonic fibroblasts, cancer cells, and laryngeal squamous cell carcinoma (LSCC) clinical samples was examined by quantitative real-time PCR (qRT–PCR), western blotting, immunofluorescence (IF), and immunohistochemistry. Extensive in vitro and in vivo experiments were carried out to determine the role of ERO1α and its downstream target, member 11 of the solute carrier family 7 (SLC7A11), in mTORC1-mediated cell proliferation, angiogenesis, ferroptosis resistance, and tumor growth. The regulatory mechanism of ERO1α on SLC7A11 was investigated via RNA-sequencing, a cytokine array, an enzyme-linked immunosorbent assay, qRT–PCR, western blotting, IF, a luciferase reporter assay, and a chromatin immunoprecipitation assay. The combined therapeutic effect of ERO1α inhibition and the ferroptosis inducer imidazole ketone erastin (IKE) on mTORC1-activated cells was evaluated using cell line-derived xenografts, LSCC organoids, and LSCC patient-derived xenograft models. Results ERO1α is a functional downstream target of mTORC1. Elevated ERO1α induced ferroptosis resistance and exerted pro-oncogenic roles in mTORC1-activated cells via upregulation of SLC7A11. Mechanically, ERO1α stimulated the transcription of SLC7A11 by activating the interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) pathway. Moreover, ERO1α inhibition combined with treatment using the ferroptosis inducer IKE exhibited synergistic antitumor effects on mTORC1-activated tumors. Conclusions The ERO1α/IL-6/STAT3/SLC7A11 pathway is crucial for mTORC1-mediated ferroptosis resistance and tumor growth, and combining ERO1α inhibition with ferroptosis inducers is a novel and effective treatment for mTORC1-related tumors.

Abstract Background Although hepatitis B virus (HBV) infection is a major risk factor for hepatic cancer, the majority of HBV carriers do not develop this lethal disease. Additional molecular alterations are thus implicated in the process of liver tumorigenesis. Since phosphatase and tensin homolog (PTEN) is decreased in approximately half of liver cancers, we investigated the significance of PTEN deficiency in HBV-related hepatocarcinogenesis. Methods HBV-positive human liver cancer tissues were checked for PTEN expression. Transgenic HBV, Alb-Cre and Pten fl/fl mice were inter-crossed to generate WT, HBV, Pten −/− and HBV; Pten −/− mice. Immunoblotting, histological analysis and qRT-PCR were used to study these livers. Gp73 −/− mice were then mated with HBV; Pten −/− mice to illustrate the role of hepatic tumor biomarker golgi membrane protein 73 (GP73)/ golgi membrane protein 1 (GOLM1) in hepatic oncogenesis. Results Pten deletion and HBV transgene synergistically aggravated liver injury, inflammation, fibrosis and development of mixed hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). GP73 was augmented in HBV; Pten −/− livers. Knockout of GP73 blunted the synergistic effect of deficient Pten and transgenic HBV on liver injury, inflammation, fibrosis and cancer development. Conclusions This mixed HCC-ICC mouse model mimics liver cancer patients harboring HBV infection and PTEN/AKT signaling pathway alteration. Targeting GP73 is a promising therapeutic strategy for cancer patients with HBV infection and PTEN alteration.

Abstract Intestinal ischemia-reperfusion (I/R) is a multifaceted pathological process, and there is a lack of clear treatment for intestinal I/R injury. During intestinal I/R, oxidative stress and inflammation triggered by cells can trigger a variety of cell death mechanisms, including apoptosis, autophagy, pyroptosis, ferroptosis, and necrosis. These cell death processes can send a danger signal for the body to be damaged and prevent intestinal I/R injury. Therefore, identifying key regulatory molecules or markers of these cell death mechanisms when intestinal I/R injury occurs may provide valuable information for the treatment of intestinal I/R injury. This paper reviews the regulatory molecules and potential markers that may be involved in regulating cell death during intestinal I/R and elaborates on the cell death mechanism of intestinal I/R injury at the molecular level to provide a theoretical basis for discovering new molecules or markers regulating cell death during intestinal I/R injury and provides ideas for drug development for the treatment of intestinal I/R injury.

BackgroundBreast cancer (BC) is one of the most frequently observed malignancies globally, yet drug development for BC has been encountering escalating challenges. Commiphora myrrha is derived from the dried resin of C. myrrha (T. Nees) Engl., and is widely adopted in China for treating BC. However, the anti-BC effect and underlying mechanism of C. myrrha remain largely unclear.MethodsMTT assay, EdU assay, and colony formation were used to determine the effect of C. myrrha n-hexane extract (CMHE) on the proliferation of human BC cells. Cell cycle distribution and apoptosis were assessed via flow cytometry analysis. Moreover, metastatic potential was evaluated using wound-scratch assay and matrigel invasion assay. The 4T1 breast cancer-bearing mouse model was established to evaluate the anti-BC efficacy of CMHE in vivo. RNA-sequencing analysis, quantitative real-time PCR, immunoblotting, immunohistochemical analysis, RNA interference assay, and database analysis were conducted to uncover the underlying mechanism of the anti-BC effect of CMHE.ResultsWe demonstrated the significant inhibition in the proliferative capability of BC cell lines MDA-MB-231 and MCF-7 by CMHE. Moreover, CMHE-induced G0/G1 phase arrest and apoptosis of the above two BC cell lines were also observed. CMHE dramatically repressed the metastatic potential of these two cells in vitro. Additionally, the administration of CMHE remarkably suppressed tumor growth in 4T1 tumor–bearing mice. No obvious toxic or side effects of CMHE administration in mice were noted. Furthermore, immunohistochemical (IHC) analysis demonstrated that CMHE treatment inhibited the proliferative and metastatic abilities of cancer cells, while also promoting apoptosis in the tumor tissues of mice. Based on RNA sequencing analysis, quantitative real-time PCR, immunoblotting, and IHC assay, the administration of CMHE downregulated Cyclin D1/CDK4-Rb signaling pathway in BC. Furthermore, RNA interference assay and database analysis showed that downregulated Cyclin D1/CDK4 signaling cascade participated in the anti-BC activity of CMHE.ConclusionCMHE treatment resulted in the suppression of BC cell growth through the stimulation of cell cycle arrest at the G0/G1 phase and the induction of apoptotic cell death via the inhibition of the Cyclin D1/CDK4-Rb pathway, thereby enhancing the anti-BC effect of CMHE. CMHE has potential anti-BC effects, particularly in those harboring aberrant activation of Cyclin D1/CDK4-Rb signaling.

Abstract Background Usenamine A, a novel natural compound initially isolated from the lichen Usnea longissima, has exhibited promising efficacy against hepatoma in prior investigation. Nevertheless, the underlying mechanisms responsible for its antihepatoma effects remain unclear. Furthermore, the role of the AKT/mechanistic target of the rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3)/inhibitor of differentiation/DNA binding 1 (ID1) signaling axis in hepatocellular carcinoma (HCC), and the potential anti-HCC effects of drugs targeting this pathway are not well understood. Methods CCK-8 assay was used to investigate the effects of usenamine A on the proliferation of human HCC cells. Moreover, the effects of usenamine A on the invasion ability of human HCC cells were evaluated by transwell assay. In addition, expression profiling analysis, quantitative real-time PCR, immunoblotting, immunohistochemistry (IHC) analysis, RNAi, immunoprecipitation, and chromatin immunoprecipitation (ChIP) assay were used to explore the effects of usenamine A on the newly identified AKT/mTOR/STAT3/ID1 signaling axis in human HCC cells. Results Usenamine A inhibited the proliferation and invasion of human HCC cell lines (HepG2 and SK-HEP-1). Through the analysis of gene expression profiling, we identified that usenamine A suppressed the expression of ID1 in human HCC cells. Furthermore, immunoprecipitation experiments revealed that usenamine A facilitated the degradation of the ID1 protein via the ubiquitin–proteasome pathway. Moreover, usenamine A inhibited the activity of STAT3 in human HCC cells. ChIP analysis demonstrated that STAT3 positively regulated ID1 expression at the transcriptional level in human HCC cells. The STAT3/ID1 axis played a role in mediating the anti-proliferative and anti-invasive impacts of usenamine A on human HCC cells. Additionally, usenamine A suppressed the STAT3/ID1 axis through AKT/mTOR signaling in human HCC cells. Conclusion Usenamine A displayed robust anti-HCC potential, partly attributed to its capacity to downregulate the AKT/mTOR/STAT3/ID1 signaling pathway and promote ubiquitin–proteasome-mediated ID1 degradation. Usenamine A has the potential to be developed as a therapeutic agent for HCC cases characterized by abnormal AKT/mTOR/STAT3/ID1 signaling, and targeting the AKT/mTOR/STAT3 signaling pathway may be a viable option for treating patients with HCC exhibiting elevated ID1 expression.

Low-temperature freezing stress constitutes the most significant meteorological disaster during the overwintering period in the Nanfeng Tangerine (NT) production area, severely impacting the normal growth and development of the plants. Currently, the accuracy of meteorological disaster warnings and forecasts for NT orchards remains suboptimal, primarily due to the absence of quantitative meteorological indicators for low-temperature freezing stress. Therefore, this study employed NT plants as experimental subjects and conducted controlled treatment experiments under varying intensities of low-temperature freezing stress (0 °C, −2 °C, −5 °C, −7 °C, and −9 °C) and durations (1 h, 4 h, and 7 h). Subsequently, physiological and biochemical parameters were measured, including photosynthetic parameters, chlorophyll fluorescence parameters, reactive oxygen species, osmoregulatory substances, and antioxidant enzyme activities in NT plants. The results demonstrated that low-temperature freezing stress adversely affected the photosynthetic system of NT plants, disrupted the dynamic equilibrium of the antioxidant system, and compromised cellular stability. The severity of freezing damage increased with decreasing temperature and prolonged exposure. Chlorophyll (a/b) ratio (Chl (a/b)), maximum quantum yield of photosystem II (Fv/Fm), soluble sugar, and malondialdehyde (MDA) were identified as key indicators for assessing physiological and biochemical changes in NT plants. Utilizing these four parameters, a comprehensive score (CS) model of freezing damage was developed to quantitatively evaluate the growth status of NT plants across varying low-temperature freezing damage gradients and durations. Subsequently, the freezing damage grade index for NT plants during the overwintering period was established. Specifically, Level 1 for CS ≤ −0.50, Level 2 for −0.5 < CS ≤ 0, Level 3 for 0 < CS ≤ 0.5, and Level 4 for 0.5 < CS. The research results provide valuable data for agricultural meteorological departments to carry out disaster monitoring, early warning, and prevention and control.

The gut microbiota, known as the “forgotten organ” and “human second genome,” comprises a complex microecosystem. It significantly influences the development of various tumors, including colorectal, liver, stomach, breast, and lung cancers, through both direct and indirect mechanisms. These mechanisms include the “gut-liver” axis, the “lung-intestine” axis, and interactions with the immune system. The intestinal flora exhibits dual roles in cancer, both promoting and suppressing its progression. Traditional Chinese medicine (TCM) can alter cancer progression by regulating the intestinal flora. It modifies the intestinal flora’s composition and structure, along with the levels of endogenous metabolites, thus affecting the intestinal barrier, immune system, and overall body metabolism. These actions contribute to TCM’s significant antitumor effects. Moreover, the gut microbiota metabolizes TCM components, enhancing their antitumor properties. Therefore, exploring the interaction between TCM and the intestinal flora offers a novel perspective in understanding TCM’s antitumor mechanisms. This paper succinctly reviews the association between gut flora and the development of tumors, including colorectal, liver, gastric, breast, and lung cancers. It further examines current research on the interaction between TCM and intestinal flora, with a focus on its antitumor efficacy. It identifies limitations in existing studies and suggests recommendations, providing insights into antitumor drug research and exploring TCM’s antitumor effectiveness. Additionally, this paper aims to guide future research on TCM and the gut microbiota in antitumor studies.

Abstract Ferroptosis is a non-apoptotic form of regulated cell death characterized by iron-dependent lipid peroxidation. It can be triggered by various mechanisms, including the glutathione peroxidase 4 (GPX4)-glutathione (GSH) axis, iron metabolism, lipid metabolism, the GTP cyclohydrolase 1 (GCH1)-tetrahydrobiopterin (BH4) pathway, and the ferroptosis suppressor protein 1 (FSP1)-coenzyme Q10 axis. The redox balance is disrupted when ferroptosis occurs in cells, which is fatal to cancer cells. Additionally, some tumor-associated genes are involved in ferroptosis. Hence, targeting ferroptosis might be an effective strategy for treating cancer. Several small-molecule compounds exhibit anti-tumor effects through ferroptosis, including sorafenib and altretamine, which induce ferroptosis by inhibiting System-Xc and GPX4 respectively, but many problems, such as poor druggability, still exist. Some studies have shown that many traditional Chinese medicine (TCM) induce ferroptosis by inhibiting GPX4, solute carrier family 7 member 11 (SLC7A11), and nuclear factor (erythroid-derived 2)-like 2 (Nrf2), or by increasing the expression of Acyl-CoA synthetase long-chain family member 4 (ACSL4), transferrin (TF), and transferrin receptor 1 (TFR1). These changes can lead to the lysosomal degradation of ferritin, accumulation of iron, lipid peroxidation and the production of reactive oxygen species (ROS), which in turn can promote anti-tumor activities or synergistic effects with chemotherapeutic drugs. In this study, we elucidated the underlying mechanisms of ferroptosis, and the anti-tumor pharmacology of TCM targeting ferroptosis including prescriptions, Chinese herbs, extracts, and natural compounds. Our findings might act as valuable reference for research on anti-tumor drugs targeting ferroptosis, especially those drugs developed from TCM.

Hepatocellular carcinoma (HCC) is a major global cause of carcinoma-related fatality. The inhibition of tubulin polymerization holds significant potential in the development of cancer drugs. In our study, we synthesized a novel pyrrolidine-2,5-dione derivative (compound 8) that exhibited potent anti-HCC activity (IC50 value of 2.082 μM) against human HCC HepG2 cells. Moreover, compound 8 significantly suppressed the HepG2 cell multiplication, and triggered G2/M phase arrest of HepG2 cells and their apoptosis. Further mechanistic investigations revealed that compound 8 suppressed tubulin polymerization by directly binding to the colchicine binding site of β-tubulin. Additionally, compound 8 significantly inhibited tumor growth with low toxicity in nude HepG2 tumor-bearing mice, achieving an approximate inhibition rate of 45.73 %. Therefore, compound 8 represents a promising pharmaceutical candidate for HCC management.

Cold stress seriously inhibits plant growth and development, geographical distribution, and yield stability of plants. Cold acclimation (CA) is an important strategy for modulating cold stress, but the mechanism by which CA induces plant resistance to cold stress is still not clear. The purpose of this study was to investigate the effect of CA treatment on the cold resistance of citrus seedlings under cold stress treatment, and to use seedlings without CA treatment as the control (NA). The results revealed that CA treatment increased the content of photosynthetic pigments under cold stress, whereas cold stress greatly reduced the value of gas exchange parameters. CA treatment also promoted the activity of Rubisco and FBPase, as well as led to an upregulation of the transcription levels of photosynthetic related genes (rbcL and rbcS)，compared to the NA group without cold stress. In addition, cold stress profoundly reduced photochemical chemistry of photosystem II (PSII), especially the maximum quantum efficiency (Fv/Fm) in PSII. Conversely, CA treatment improved the chlorophyll a fluorescence parameters, thereby improving electron transfer efficiency. Moreover, under cold stress, CA treatment alleviated oxidative stress damage to cell membranes by inhibiting the concentration of H2O2 and MDA, enhancing the activities of superoxide dismutase (SOD), catalase (CAT), ascorbic acid peroxidase (APX) and glutathione reductase (GR), accompanied by an increase in the expression level of antioxidant enzyme genes (CuZnSOD1, CAT1, APX and GR). Additionally, CA also increased the contents of abscisic acid (ABA) and salicylic acid (SA) in plants under cold stress. Overall, we concluded that CA treatment suppressed the negative effects of cold stress by enhancing photosynthetic performance, antioxidant enzymes functions and plant hormones contents.

High temperatures significantly injure the flowering, pollination, fruit growth, and quality of plants. Photosynthesis, the fundamental process supporting plant life, is crucial. Nevertheless, the quantitative evaluation of the physiological activity of the photosynthetic system of Nanfeng tangerine (NT) plants under high-temperature conditions remains a challenge. This research utilized NT plants, a distinctive citrus variety in Jiangxi Province, as the experimental subject. The study investigated the effects of varying degrees of high-temperature stress and duration on 16 photosynthetic physiological parameters of NT plants. The study examined the impact of four varying high-temperature treatment levels (32/22 °C, 35/25 °C, 38/28 °C, and 41/31 °C) for durations of 2, 4, 6, and 8 days, respectively. Principal component analysis was utilized to identify the key indicators of photosynthetic physiological activity in NT plants, with Fv/Fm, Pmax, LCP, H2O2, MDA, and POD being selected as key parameters. The high-temperature stress index model previously constructed was used to calculate the high-temperature stress index value of the NT plants exposed to varying degrees and durations of high temperature, in order to provide a comprehensive assessment of the photosynthetic system of NT plants under high-temperature stress. Subsequently, the high-temperature stress levels were categorized into five levels based on the calculated values: Level 0 for 0 < HSI ≤ 2, Level 1 for 2 < HSI ≤ 4, Level 2 for 4 < HSI ≤ 6, Level 3 for 6 < HSI ≤ 8, and Level 4 for HSI > 8. The research results provide valuable data for agricultural meteorological departments to carry out disaster risk zoning and risk assessment in the future.

Polygonatum cyrtonema Hua (family Asparagaceae) is an endemic plant in China that is valuable for its edible and medicinal uses. Plant growth regulators (PGRs) are natural or synthetic compounds that can regulate plant development and metabolism effectively. To explore potential applications of PGRs for improving the yield and bioactivity of this plant, four PGRs, including gibberellic acid (GA3), 6-benzylaminopurine (6-BA), naphthaleneacetic acid (NAA) and 24-epibrassinolide (EBL), were used in this study and sprayed on the growing seedlings of P. cyrtonema. All of these PGRs did not significantly affect the growth rate of P. cyrtonema, but they had varying effects on the polysaccharide and saponin content in the rhizome. NAA and 6-BA positively affected the polysaccharide content, while most PGR treatments negatively affected the saponin content. Widely targeted metabolomic analysis based on UPLC-MS/MS was conducted and revealed 101 differential metabolites in response to 6-BA, most of which were flavonoids, steroids and lipids. Most of the significantly changed flavonoids decreased under the 6-BA treatment. The study provides insights into the potential use of PGRs for improving the quality of P. cyrtonema, particularly in regulating the content of bioactive compounds.

Abstract As evidenced by the behavior of loss-of-function mutants of PTEN in the context of a gain-of-function mutation of AKT1, the PTEN-AKT1 signaling pathway plays a critical role in human cancers. In this study, we demonstrated that a deficiency in PTEN or activation of AKT1 potentiated the expression of platelet-derived growth factor receptor α (PDGFRα) based on studies on Pten−/− mouse embryonic fibroblasts, human cancer cell lines, the hepatic tissues of Pten conditional knockout mice, and human cancer tissues. Loss of PTEN enhanced PDGFRα expression via activation of the AKT1-CREB signaling cascade. CREB transactivated PDGFRα expression by direct binding of the promoter of the PDGFRα gene. Depletion of PDGFRα attenuated the tumorigenicity of Pten-null cells in nude mice. Moreover, the PI3K-AKT signaling pathway has been shown to positively correlate with PDGFRα expression in multiple cancers. Augmented PDGFRα was associated with poor survival of cancer patients. Lastly, combination treatment with the AKT inhibitor MK-2206 and the PDGFR inhibitor CP-673451 displayed synergistic anti-tumor effects. Therefore, activation of the AKT1-CREB-PDGFRα signaling pathway contributes to the tumor growth induced by PTEN deficiency and should be targeted for cancer treatment.

The mandarin is an important fruit crop worldwide, and ‘Xinyu mandarin’—a local Citrus reticulata variety—is widely cultivated in Jiangxi Province, in China. Autopolyploidy has frequently been used for the improvement of crop varieties. In a previous study, we identified a tetraploid (4X) material of ‘Xinyu mandarin’ generated from its diploid (2X) mother seedling via a spontaneous mutation. However, the physiological and metabolic variations after polyploidy are not clear enough, which is not conducive to the early screening. In the present study, we analyzed the morphological, physiological, and metabolic differences between the tetraploid and diploid plants. The tetraploids had larger and thicker leaves, and the activities of key enzymes in photosynthesis, the total chlorophyll, phenolic, and proline contents, were all higher in tetraploids. In the non-targeted metabolomic profile, a total of 522 metabolites were identified, of which 61 were significantly different between diploids and tetraploids. The differential metabolites included similar proportions of primary and secondary metabolites, and most of these were up-regulated in tetraploids, especially stress-related metabolites such as phenolic acids, flavonoids, alkaloids, and so on, indicating that tetraploids may possess better stress tolerance ability and vigor. Therefore, the tetraploids of ‘Xinyu mandarin’ may serve as an excellent female parent for the improvement of citrus varieties.

Aiming at the shortages of basic flower pollination algorithm (FPA) with slow convergence speed, low search precision, and easy to fall into local optimum, a new adaptive FPA based on opposition-based learning and t-distribution (OTAFPA) was proposed and be applied to the social networks. First, the opposition-based learning strategy is utilized to increase the diversity and quality of the initial population. Then, the adaptive dynamic switching probability is introduced, which can effectively balance the global and local search according to the current number of iterations. Finally, the t-distribution variation is used to increase the population diversity and to help the algorithm jump out of the local optimum. The simulation experiments on eight classical test functions show that OTAFPA has better global optimization ability, which improves the convergence speed and the solution accuracy of the algorithm. The OTAFPA also shows superior performance in practical applications of user identification across social networks.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies, which ranks the third leading cause of cancer-related death worldwide. The screening of anti-HCC drug with high efficiency and low toxicity from traditional Chinese medicine (TCM) has attracted more and more attention. As a TCM, Chinese dragon’s blood has been used for the treatment of cardiovascular illness, gynecological illness, skin disorder, otorhinolaryngological illness, and diabetes mellitus complications for many years. However, the anti-tumor effect and underlying mechanisms of Chinese dragon’s blood remain ill-defined. Herein we have revealed that Chinese dragon’s blood EtOAc extract (CDBEE) obviously suppressed the growth of human hepatoma HepG2 and SK-HEP-1 cells. Moreover, CDBEE inhibited the migration and invasion of HepG2 and SK-HEP-1 cells. Additionally, CDBEE displayed good in vitro anti-angiogenic activity. Importantly, CDBEE treatment significantly blunted the oncogenic capability of HepG2 cells in nude mice. Mechanistically, CDBEE inhibited Smad3 expression in human hepatoma cells and tumor tissues from nude mice. Using RNA interference, we demonstrated that CDBEE exerted anti-hepatoma activity partially through down-regulation of Smad3, one of major members in TGF-β/Smad signaling pathway. Therefore, CDBEE may be a promising candidate drug for HCC treatment, especially for liver cancer with aberrant TGF-β/Smad signaling pathway.

Abstract Since the incidence of cancer has been on the rise due to increasing exposure to various carcinogenic factors in recent years, cancer has gradually become the first killer to the health of human beings. A growing attention has been paid to anti-cancer effects of traditional Chinese medicine (TCM) with low toxicity and good efficacy. As a kind of TCM, Periplaneta americana (P. americana) has a good effect on clinical application, and its anti-tumor effects has been increasingly well studied. In this review, the research progress on the anti-tumor effects of P. americana was summarized. The main mechanisms of its anti-tumor effects include suppression of tumor cell growth, induction of cell cycle arrest and tumor cell apoptosis, inhibition of angiogenesis, enhancement of immunity, and reversal of tumor drug resistance. This review aims to provide an overview of the research on anti-tumor effects of P. americana and aids in its further application as an anti-tumor drug.

Aiming at the problem of wireless sensor network node coverage optimization with obstacles in the monitoring area, based on the grey wolf optimizer algorithm, this paper proposes an improved grey wolf optimizer (IGWO) algorithm to improve the shortcomings of slow convergence, low search precision, and easy to fall into local optimum. Firstly, the nonlinear convergence factor is designed to balance the relationship between global search and local search. The elite strategy is introduced to protect the excellent individuals from being destroyed as the iteration proceeds. The original weighting strategy is improved, so that the leading wolf can guide the remaining grey wolves to prey in a more reasonable way. The design of the grey wolf’s boundary position strategy and the introduction of dynamic variation strategy enrich the population diversity and enhance the ability of the algorithm to jump out of local optimum. Then, the benchmark function is used to test the convergence performance of genetic algorithm, particle swarm optimization, grey wolf optimizer, and IGWO algorithm, which proves that the convergence performance of IGWO algorithm is better than the other three algorithms. Finally, the IGWO algorithm is applied to the deployment of wireless sensor networks with obstacles (rectangular obstacle, trapezoidal obstacle and triangular obstacles). Simulation results show that compared with GWO algorithm, IGWO algorithm can effectively improve the coverage of wireless sensor network nodes and obtain higher coverage rate with fewer nodes, thereby reducing the cost of deploying the network.

Non-destructive phenotyping of roots and measurement of root water uptake from different soil layers in the field are vital for improving water management and facilitating the development of drought-resistant crop varieties, but difficult because of their opaqueness. As a result, indirect methods using easy-to-measure variables such as soil water content have been used as alternatives. However, the inherent measurement errors could undermine the robustness and reliability of these methods. This paper proposes a new method to bridge this knowledge gap by using soil water content profiles measured at two time points to calculate root uptake and root-length density. It is based on the Richards' equation by treating root uptake from different soil layers between the two time points as random unknown numbers; their distributions are calculated using the Bayesian framework, solved by the Markov Chain Monte Carlo method. We applied the method to 39 winter wheat lines grown in a silt-clay loam field. Soil water content profile measured at the first time point from each plot served as the initial condition, and water content measured at the second time point was the target to match the model for calculating average root water uptake and root-length density between the two time points. The results show that the measured soil water contents fall within the 95% confidence interval of the calculated soil water contents. The inherent soil water measurement errors lead to uncertainties in the calculated root water uptake for all lines, but such uncertainties decrease with soil depth. Although the soil types and agronomic management were the same for all 39 lines, their root water uptake from different soil layers varies considerably, with some lines more capable of using subsoil water than others. Generally, the calculated and measured root-length densities agree well, albeit the degree of the agreement varies with lines. While this paper focuses on methodology and applies the method to one growth stage spanning one month only, the consistent results for all 39 lines indicates the method is robust and can be applied to other crops cultivated in different conditions. Given the growing interest in improving root traits to enhance water use efficiency, the proposed method has important implications as phenotyping roots and understanding their water uptake from different soil layers in the field is a prerequisite to achieve this crucial target.