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Ethnopharmacological Relevance: Cervical cancer (CC) is a potentially lethal disorder that can have serious consequences for a woman's health. Because early symptoms are typically only present in the middle to late stages of the disease, clinical diagnosis and treatment can be challenging. Traditional Chinese medicine (TCM) has been shown to have unique benefits in terms of alleviating cancer clinical symptoms, lowering the risk of recurrence after surgery, and reducing toxic side effects and medication resistance after radiation therapy. It has also been shown to improve the quality of life for patients. Because of its improved anti-tumor effectiveness and biosafety, it could be considered an alternative therapy option. This study examines how TCM causes apoptosis in CC cells via signal transduction, including the active components and medicinal tonics. It also intends to provide a reliable clinical basis and protocol selection for the TCM therapy of CC., Methods: The following search terms were employed in PubMed, Web of Science, Embase, CNKI, Wanfang, VIP, SinoMed, and other scientific databases to retrieve pertinent literature on "cervical cancer," "apoptosis," "signaling pathway," "traditional Chinese medicine," "herbal monomers," "herbal components," "herbal extracts," and "herbal formulas.", Results: It has been demonstrated that herbal medicines can induce apoptosis in cells of the cervix, a type of cancer, by influencing the signaling pathways involved., Conclusion: A comprehensive literature search was conducted, and 148 papers from the period between January 2017 and December 2023 were identified as eligible for inclusion. After a meticulous process of screening, elimination and summary, generalization, and analysis, it was found that TCM can regulate multiple intracellular signaling pathways and related molecular targets, such as STAT3, PI3K/AKT, Wnt/β-catenin, MAPK, NF-κB, p53, HIF-1α, Fas/FasL and so forth. This regulatory capacity was observed to induce apoptosis in cervical cancer cells. The study of the mechanism of TCM against cervical cancer and the screening of new drug targets is of great significance for future research in this field. The results of this study will provide ideas and references for the future development of Chinese medicine in the diagnosis and treatment of cervical cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

ent -Kaur-15-en-17-al-18-oic acid, extracted from the Chinese well known folk herb Leontopodium longifolium , performed a significantly neuroprotective effect on amyloid beta peptide 25-35 (Aβ 25-35 )-induced SH-SY5Y cells neurotoxicity in Alzheimer's disease. The results demonstrated that this compound maintained oxidative stress balance, reduced levels of reactive oxygen species (ROS), malondialdehyde (MDA), and improved contents of glutathione (GSH) and superoxide dismutase (SOD) without obvious cytotoxicity. This compound also obviously relieved oxidative stress-induced apoptosis associated with p53 and nuclear factor κB (NF-κB) pathways accompanied by upregulating B-cell lymphoma-2 (bcl-2) and downregulating p53, nuclear factor κB (NF-κB), Bax, Cleaved-caspase 3, and Cytochrome C protein expressions further. Briefly, ent -kaur-15-en-17-al-18-oic acid protected cells from oxidative apoptosis associated with p53 and NF-κB pathways.

Background and Objectives : Microtubules are an attractive target for cancer chemotherapy. Previously, we reported that Ivalin exhibited excellent anti-migration and anti-invasion activities in human breast cancer cells. Here, we examined the microtubule inhibition effect of Ivalin in human hepatocellular carcinoma SMMC-7721 cells. Materials and Methods : We used the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay to evaluate the cell proliferation effect of Ivalin and flow cytometry analysis to detect the apoptotic and cell cycle arrest effects of Ivalin. Immunofluorescence staining was used to measure the effect of Ivalin on the cytoskeleton network, and Western blotting was used to detect the expression levels of Bax, Bcl-2, Cdc2, phosphor-Cdc2, Cdc25A, Cyclin B1, and tubulin. Results : Ivalin induced cell cycle G2/M arrest and subsequent triggered apoptosis in human hepatocellular carcinoma SMMC-7721 cells. Furthermore, microtubules were shown to be involved in Ivalin-meditated apoptosis. In this connection, Ivalin treatment suppressed cellular microtubule network formation by regulating microtubule depolymerization. Moreover, Western blotting revealed Cdc25A and Cyclin B1 were upregulated in Ivalin-meditated cell cycle arrest. Subsequently, the induction of Bax (a proapoptotic protein) and reduction of Bcl-2 (an anti-apoptotic protein) expression were observed in Ivalin-treated SMMC-7721 cells. Conclusion : Ivalin induced microtubule depolymerization, then blocked cells in mitotic phase, and eventually resulted in apoptosis in SMMC-7721 cells. Collectively, these data indicate that Ivalin, acting as a novel inhibitor of microtubules, could be considered as a promising lead in anticancer drug development.

Oxidative stress (OS)-induced retinal pigment epithelium (RPE) cell apoptosis is critically implicated in the pathogenesis of age-related macular degeneration (AMD), a leading cause of blindness in the elderly. Heterochromatin, a compact and transcriptional inert chromatin structure, has been recently shown to be dynamically regulated in response to stress stimuli. The functional mechanism of heterochromatin on OS exposure is unclear, however. Here we show that OS increases heterochromatin formation both in vivo and in vitro, which is essential for protecting RPE cells from oxidative damage. Mechanistically, OS-induced heterochromatin selectively accumulates at p53-regulated proapoptotic target promoters and inhibits their transcription. Furthermore, OS-induced desumoylation of p53 promotes p53-heterochromatin interaction and regulates p53 promoter selection, resulting in the locus-specific recruitment of heterochromatin and transcription repression. Together, our findings demonstrate a protective function of OS-induced heterochromatin formation in which p53 desumoylation-guided promoter selection and subsequent heterochromatin recruitment play a critical role. We propose that targeting heterochromatin provides a plausible therapeutic strategy for the treatment of AMD., Competing Interests: The authors declare no conflict of interest., (Copyright © 2018 the Author(s). Published by PNAS.)

Doxorubicin (DOX) is a chemotherapeutic drug widely used in the field of cancer, but its side effects on the heart hinder its clinical application. In cardiac injury caused by DOX, apoptosis and oxidative stress are both involved in cardiac damage, and autophagy is also one of the key responses. Both apoptosis and oxidative stress interact with autophagy. Proper promotion of autophagy effectively protects the myocardium and blocks cardiac injury. DOX mainly acts downstream of the autophagic flow and hinders the degradation process of autophagolysosomes, resulting in abnormal accumulation of autophagolysosomes in cells, which can prevent the timely removal of harmful substances and disrupt the normal function of cells. Proprotein convertase subtilisin/kexin type 6 (PCSK6) is involved in the occurrence and development of various cardiovascular diseases, blood pressure regulation and the inflammatory response, but its role in DOX is still unclear. Here, we constructed cardiac PCSK6-overexpressing mice by injecting AAV9-PCSK6. Both in vivo and in vitro experiments confirmed that overexpression of PCSK6 effectively protected cardiac function, inhibited apoptosis and oxidative stress. We focused on the effect of PCSK6 overexpression on autophagy. We have detected an increase in autophagosomes production and a decrease in autophagolysosomes accumulation. This suggests that PCSK6 promotes the level of autophagy, while possibly acting on the sites where DOX inhibits degradation, so that the autophagic flux inhibited by DOX is restored and the degradation process of autophagolysosomes is restored. The effect of PCSK6 was dependent on FOXO3a, which promoted the nuclear translocation of Forkhead box O3 (FOXO3a), and Sirtuin 1 (SIRT1) regulated the expression of FOXO3a. When SIRT1 was inhibited, the protective effect of PCSK6 was diminished. In conclusion, overexpression of PCSK6 exerts a protective effect through SIRT1/FOXO3a in cardiac injury induced by DOX, suggesting that PCSK6 may be a therapeutic target for DOX cardiomyopathy. [Display omitted] • PCSK6 protected the heart from long-term damage induced by DOX. • PCSK6 attenuated cardiac oxidative stress and apoptosis levels, restored the autophagolysosome degradation process. • This protective effect of PCSK6 is achieved by regulating the SIRT1/FOXO3a signaling pathway. [ABSTRACT FROM AUTHOR]

ent-Kaur-15-en-17-al-18-oic acid, extracted from the Chinese well known folk herb Leontopodium longifolium, performed a significantly neuroprotective effect on amyloid beta peptide 25-35 (Aβ25-35)-induced SH-SY5Y cells neurotoxicity in Alzheimer's disease. The results demonstrated that this compound maintained oxidative stress balance, reduced levels of reactive oxygen species (ROS), malondialdehyde (MDA), and improved contents of glutathione (GSH) and superoxide dismutase (SOD) without obvious cytotoxicity. This compound also obviously relieved oxidative stress-induced apoptosis associated with p53 and nuclear factor κB (NF-κB) pathways accompanied by upregulating B-cell lymphoma-2 (bcl-2) and downregulating p53, nuclear factor κB (NF-κB), Bax, Cleaved-caspase 3, and Cytochrome C protein expressions further. Briefly, ent-kaur-15-en-17-al-18-oic acid protected cells from oxidative apoptosis associated with p53 and NF-κB pathways. [ABSTRACT FROM AUTHOR]

Four angucycline glycosides including three new compounds landomycin N (1), galtamycin C (2) and vineomycin D (3), and a known homologue saquayamycin B (4), along with two alkaloids 1-acetyl-β-carboline (5) and indole-3-acetic acid (6), were isolated from the fermentation broth of an intertidal sediments-derived Streptomyces sp. Their structures were established by IR, HR-ESI-MS, 1D and 2D NMR techniques. Among the isolated angucyclines, saquayamycin B (4) displayed potent cytotoxic activity against hepatoma carcinoma cells HepG-2, SMMC-7721 and plc-prf-5, with IC50 values 0.135, 0.033 and 0.244 μM respectively, superior to doxorubicin. Saquayamycin B (4) also induced apoptosis in SMMC-7721 cells as detected by its morphological characteristics in 4′,6-diamidino-2-phenylindole (DAPI) staining experiment. [ABSTRACT FROM AUTHOR]

As a "silent killer" that threatens women's lives and health, ovarian cancer (OC) has the clinical characteristics of being difficult to detect, difficult to treat, and high recurrence. Traditional Chinese medicine (TCM) can be utilized as a long-term complementary and alternative therapy since it has shown benefits in alleviating clinical symptoms of OC, decreasing toxic side effects of radiation and chemotherapy, as well as enhancing patients' quality of life. This paper reviews how TCM contributes to the apoptosis of OC cells through signaling pathways, including active constituents, extracts, and herbal formulas, with the aim of providing a basis for the development and clinical application of therapeutic strategies for TCM in OC. The search was conducted from scientific databases PubMed, Embase, Web of Science, CNKI, Wanfang, VIP, and SinoMed databases aiming to elucidate the apoptosis signaling pathways in OC cells by TCM. The articles were searched by the keywords "ovarian cancer", "apoptosis", "signaling pathway", "traditional Chinese medicine", "Chinese herbal monomer", "Chinese herbal extract", and "herbal formula". The search was conducted from January 2013 to June 2023. A total of 97 potentially relevant articles were included, including 93 articles on Chinese medicine active constituents or extracts and 4 articles on Chinese herbal compound prescriptions. TCM can induce apoptosis in OC cells by regulating signaling pathways with obvious advantages, including STAT3, PI3K/AKT, Wnt/β-catenin, MAPK, NF-κB, Nrf2, HIF-1α, Fas/Fas L signaling pathway, etc. Chinese medicine can induce apoptosis in OC cells through multiple pathways, targets, and routes. TCM has special advantages for treating OC, providing more reasonable evidence for the research and development of new apoptosis inducers. [Display omitted] [ABSTRACT FROM AUTHOR]