Fengjuan Han

Research progress on the application of traditional Chinese medicine in regulating NF-κB signaling pathway for the treatment of ovarian cancer

RNA sequencing in ovarian cancer research: a comprehensive review

Research Progress of Traditional Chinese Medicine Monomer Inhibiting Metastatic Colonization of Ovarian Cancer Cells Based on Cell Biology

Ovarian cancer, a frequently occurring gynecological malignancy with a poor prognosis and a 5-year survival rate below 45%, often progresses due to metastatic colonization. This review highlights the potential of traditional Chinese medicine (TCM) monomers as anticancer agents that inhibit the metastatic colonization of ovarian cancer cells. TCM monomers exhibit various mechanisms of action, including (1) inhibiting epithelial-to-mesenchymal transformation by modulating cell adhesion molecules; (2) reducing extracellular matrix damage through inhibition of degrading enzymes; (3) affecting cytoskeletal dynamics to alter cell movement; and (4) preventing angiogenesis by downregulating angiogenic factors. Additionally, TCM monomers can reshape the tumor microenvironment, enhance immune responses, and induce oxidative stress, resulting in reduced proliferation and survival of cancer cells. The comprehensive action of TCM monomers makes them promising candidates for individualized, multi-target therapies in drug-resistant cases. This paper reviews the current research on the mechanisms through which TCM monomers combat metastatic colonization, aiming to provide insights for future studies and clinical applications in ovarian cancer treatment, ultimately offering hope to affected patients.

Unlocking the mitochondrial functional code: unraveling the pathogenesis of ovarian cancer and innovative targets to inhibit malignant behavior

This article focuses on ovarian cancer (OC), the most lethal gynecological malignancy, whose risk is influenced by multiple factors, including genetic background, age, reproductive history, parity, obesity status, and smoking habits. Mitochondria, as the core organelles in eukaryotic cells, play a pivotal role in the initiation and progression of OC. In recent years, growing evidence has revealed a close relationship between mitochondrial dysfunction and the accelerated proliferation, enhanced invasiveness, metastasis ability, and therapy resistance of OC. This paper provides an in-depth analysis of the complex interactions between mitochondrial dysfunction and the malignant biological characteristics of OC, as well as the underlying regulatory mechanisms of mitochondrial function. Furthermore, it elaborates on how genetic variations, regulatory factors, and the tumor microenvironment (TME) influence mitochondrial function and drive the malignant progression of OC. Additionally, this paper comprehensively summarizes therapeutic strategies targeting mitochondrial dysfunction in OC, aiming to provide novel insights and strategies for clinical research and treatment.

The estrogen-progestogen-oxidative stress network in uterine fibroids: mechanistic insights and therapeutic opportunities

Uterine fibroids are benign tumors with high incidence and recurrence rates that still pose significant treatment challenges. Traditionally, it has been believed that estrogen and progesterone primarily drive the development and progression of uterine fibroids. Recent studies have revealed that hormonal imbalance can affect reactive oxygen species production and trigger a significant oxidative stress (OS) state. The OS status in uterine fibroids can further amplify the pathological effects caused by hormonal imbalance. This suggests that estrogen, progesterone, and OS may interact to form an estrogen-progesterone-oxidative stress (E-P-OS) network, collectively promoting the progression of uterine fibroids. This network model provides a theoretical basis for the high recurrence rates following hormone monotherapy or surgery. Therefore, we reviewed the molecular mechanisms underlying hormone-OS interactions within the E-P-OS network and elucidated its pathological effects in promoting uterine fibroid progression. The integrated perspective lays the theoretical foundation for developing novel therapies that simultaneously block hormone signaling and counteract oxidative damage. Additionally, we summarized current clinical strategies for hormone therapy and antioxidant treatment, identified potential combination therapy approaches, and explored key challenges in their clinical translation. This aims to provide new directions and evidence for advancing the precision treatment of uterine fibroids.

A literature review on signaling pathways of cervical cancer cell death-apoptosis induced by Traditional Chinese Medicine

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. 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." 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. 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.

Insights into the Role of Oxidative Stress in Ovarian Cancer

Oxidative stress (OS) arises when the body is subjected to harmful endogenous or exogenous factors that overwhelm the antioxidant system. There is increasing evidence that OS is involved in a number of diseases, including ovarian cancer (OC). OC is the most lethal gynecological malignancy, and risk factors include genetic factors, age, infertility, nulliparity, microbial infections, obesity, smoking, etc. OS can promote the proliferation, metastasis, and therapy resistance of OC, while high levels of OS have cytotoxic effects and induce apoptosis in OC cells. This review focuses on the relationship between OS and the development of OC from four aspects: genetic alterations, signaling pathways, transcription factors, and the tumor microenvironment. Furthermore, strategies to target aberrant OS in OC are summarized and discussed, with a view to providing new ideas for clinical treatment.

Association between XRCC3 rs861539 Polymorphism and the Risk of Ovarian Cancer: Meta‐Analysis and Trial Sequential Analysis

Background. Current studies on the relationship between XRCC3 rs861539 polymorphism and ovarian cancer risk have been inconsistent. Therefore, we performed a meta‐analysis to explore their association. Methods. Six electronic databases (PubMed, Embase, Web of Science, Cochrane Library, China National Knowledge Infrastructure, and China Wanfang Database) were searched for relevant studies published before December 2021. Meta‐analysis, subgroup analysis, sensitivity analysis, and publication bias analysis were performed using Stata software 16.0. Trial sequential analysis (TSA) was performed using TSA 0.9.5.10 Beta software. Results. A total of 12 studies were included in 9 literatures, comprising 4,634 cases of ovarian cancer and 7,381 controls. After Bonferroni correction, the meta‐analysis showed an association between XRCC3 rs861539 polymorphism and ovarian cancer risk in the heterozygote model and the dominant model (GA vs. GG: OR = 0.88, 95%CI = 0.81‐0.96, P = 0.003; GG vs. GA+AA: OR = 0.89, 95%CI = 0.82‐0.96, P = 0.004). In an ethnically stratified subgroup analysis, XRCC3 rs861539 was shown to reduce the risk of ovarian cancer in Caucasian in the heterozygote model and the dominant model (GA vs. GG: OR = 0.88, 95%CI = 0.81‐0.96, P = 0.004; GG vs. GA+AA: OR = 0.88, 95%CI = 0.81‐0.96, P = 0.004). In the control source and detection method stratified subgroup analysis, hospital‐based studies and PCR‐RFLP‐based studies were found to increase ovarian cancer risk (GG vs. AA: OR = 1.30, 95%CI = 1.05‐1.62, P = 0.016; GG vs. AA: OR = 1.31, 95%CI = 1.06‐1.62, P = 0.013). Conclusion. This meta‐analysis showed a significant association between XRCC3 rs861539 polymorphism and ovarian cancer risk, especially in Caucasians. Large‐scale multicenter case‐control studies in more different regions will be needed in the future.

The role of vaginal microecology in the cervical cancer

AbstractAimTo explore the role of vaginal microecology in cervical cancer, so as to increase the understanding of cervical cancer and lay a foundation for future large‐sample clinical trials.MethodsWe reviewed and summarized the literature comprehensively, and discussed the relationship between vaginal microecology and HPV infection, CIN progression and cervical cancer, as well as the potential molecular mechanism and the prospects of probiotics and prebiotics in future cancer treatments.ResultsWith the popularization of high‐throughput sequencing technology and the development of bioinformatics analysis technology, many evidences show that the increase in the diversity of the bacterial community in the vaginal microecological environment and the decrease in the number of Lactobacilli are associated with the continuous infection of HPV and the further development of CIN, cervical cancer‐related.ConclusionsVaginal microecological imbalance has an important impact on the occurrence and development of cervical cancer. However, the pathogenesis is not completely clear, and more high‐level basic research and longitudinal clinical studies are needed to verify.