Research progress on the premature ovarian failure caused by cisplatin therapy

Li, Zelin; Qi, Haodong; Li, Zhengyang; Bao, Yuxuan; Yang, Kangping; Min, Qinghua

doi:10.3389/fonc.2023.1276310

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…12 B, a figure from the KEGG pathway database 41 ), and the IL-17 signaling pathway. Researche shows that cisplatin reduces DNA replication and thus alleviates tumorigenesis; however, it also affects ovarian function, leading to POF 42 . Additionally, abnormalities in DNA replication can lead to the development of DED.…”

Section: Discussionmentioning

confidence: 99%

The shared mechanism and potential diagnostic markers for premature ovarian failure and dry eye disease

Long,

Wu,

Jiang

et al. 2024

Sci Rep

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Premature ovarian failure (POF), which is often comorbid with dry eye disease (DED) is a key issue affecting female health. Here, we explored the mechanism underlying comorbid POF and DED to further elucidate disease mechanisms and improve treatment. Datasets related to POF (GSE39501) and DED (GSE44101) were identified from the Gene Expression Omnibus (GEO) database and subjected to weighted gene coexpression network (WGCNA) and differentially expressed genes (DEGs) analyses, respectively, with the intersection used to obtain 158 genes comorbid in POF and DED. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses of comorbid genes revealed that identified genes were primarily related to DNA replication and Cell cycle, respectively. Protein–Protein interaction (PPI) network analysis of comorbid genes obtained the 15 hub genes: CDC20, BIRC5, PLK1, TOP2A, MCM5, MCM6, MCM7, MCM2, CENPA, FOXM1, GINS1, TIPIN, MAD2L1, and CDCA3. To validate the analysis results, additional POF- and DED-related datasets (GSE48873 and GSE171043, respectively) were selected. miRNAs-lncRNAs-genes network and machine learning methods were used to further analysis comorbid genes. The DGIdb database identified valdecoxib, amorfrutin A, and kaempferitrin as potential drugs. Herein, the comorbid genes of POF and DED were identified from a bioinformatics perspective, providing a new strategy to explore the comorbidity mechanism, opening up a new direction for the diagnosis and treatment of comorbid POF and DED.

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Section: Discussionmentioning

confidence: 99%

The shared mechanism and potential diagnostic markers for premature ovarian failure and dry eye disease

Long,

Wu,

Jiang

et al. 2024

Sci Rep

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“…Unlike standard alkylating drugs, the gynotoxic effects of platinum derivatives are considered moderately harmful. Nevertheless, in women of childbearing age treated for cancer, cisplatin can lead to impaired ovarian function, POF, and infertility [ 92 ].…”

Section: Gynotoxic Properties Of Anticancer Drugsmentioning

confidence: 99%

Gynotoxic Effects of Chemotherapy and Potential Protective Mechanisms

Markowska,

Antoszczak,

Markowska

et al. 2024

Cancers

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Chemotherapy is one of the leading cancer treatments. Unfortunately, its use can contribute to several side effects, including gynotoxic effects in women. Ovarian reserve suppression and estrogen deficiency result in reduced quality of life for cancer patients and are frequently the cause of infertility and early menopause. Classic alkylating cytostatics are among the most toxic chemotherapeutics in this regard. They cause DNA damage in ovarian follicles and the cells they contain, and they can also induce oxidative stress or affect numerous signaling pathways. In vitro tests, animal models, and a few studies among women have investigated the effects of various agents on the protection of the ovarian reserve during classic chemotherapy. In this review article, we focused on the possible beneficial effects of selected hormones (anti-Müllerian hormone, ghrelin, luteinizing hormone, melatonin), agents affecting the activity of apoptotic pathways and modulating gene expression (C1P, S1P, microRNA), and several natural (quercetin, rapamycin, resveratrol) and synthetic compounds (bortezomib, dexrazoxane, goserelin, gonadoliberin analogs, imatinib, metformin, tamoxifen) in preventing gynotoxic effects induced by commonly used cytostatics. The presented line of research appears to provide a promising strategy for protecting and/or improving the ovarian reserve in the studied group of cancer patients. However, well-designed clinical trials are needed to unequivocally assess the effects of these agents on improving hormonal function and fertility in women treated with ovotoxic anticancer drugs.

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Non-coding RNAs as potential targets in metformin therapy for cancer

Zhang,

Wu,

Liu

et al. 2024

Cancer Cell Int

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Metformin, a widely used oral hypoglycemic drug, has emerged as a potential therapeutic agent for cancer treatment. While initially known for its role in managing diabetes, accumulating evidence suggests that metformin exhibits anticancer properties through various mechanisms. Several cellular or animal experiments have attempted to elucidate the role of non-coding RNA molecules, including microRNAs and long non-coding RNAs, in mediating the anticancer effects of metformin. The present review summarized the current understanding of the mechanisms by which non-coding RNAs modulate the response to metformin in cancer cells. The regulatory roles of non-coding RNAs, particularly miRNAs, in key cellular processes such as cell proliferation, cell death, angiogenesis, metabolism and epigenetics, and how metformin affects these processes are discussed. This review also highlights the role of lncRNAs in cancer types such as lung adenocarcinoma, breast cancer, and renal cancer, and points out the need for further exploration of the mechanisms by which metformin regulates lncRNAs. In addition, the present review explores the potential advantages of metformin-based therapies over direct delivery of ncRNAs, and this review highlights the mechanisms of non-coding RNA regulation when metformin is combined with other therapies. Overall, the present review provides insights into the molecular mechanisms underlying the anticancer effects of metformin mediated by non-coding RNAs, offering novel opportunities for the development of personalized treatment strategies in cancer patients.

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Research progress on the premature ovarian failure caused by cisplatin therapy

Cited by 4 publications

References 36 publications

The shared mechanism and potential diagnostic markers for premature ovarian failure and dry eye disease

The shared mechanism and potential diagnostic markers for premature ovarian failure and dry eye disease

Gynotoxic Effects of Chemotherapy and Potential Protective Mechanisms

Non-coding RNAs as potential targets in metformin therapy for cancer

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