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Novel Players in the Development of Chemoresistance in Ovarian Cancer: Ovarian Cancer Stem Cells, Non-coding RNA and Nuclear Receptors

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Date 2024 Mar 4
PMID 38434767
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Abstract

Ovarian cancer (OC) ranks as the fifth leading factor for female mortality globally, with a substantial burden of new cases and mortality recorded annually. Survival rates vary significantly based on the stage of diagnosis, with advanced stages posing significant challenges to treatment. OC is primarily categorized as epithelial, constituting approximately 90% of cases, and correct staging is essential for tailored treatment. The debulking followed by chemotherapy is the prevailing treatment, involving platinum-based drugs in combination with taxanes. However, the efficacy of chemotherapy is hindered by the development of chemoresistance, both acquired during treatment (acquired chemoresistance) and intrinsic to the patient (intrinsic chemoresistance). The emergence of chemoresistance leads to increased mortality rates, with many advanced patients experiencing disease relapse shortly after initial treatment. This review delves into the multifactorial nature of chemoresistance in OC, addressing mechanisms involving transport systems, apoptosis, DNA repair, and ovarian cancer stem cells (OCSCs). While previous research has identified genes associated with these mechanisms, the regulatory roles of non-coding RNA (ncRNA) and nuclear receptors in modulating gene expression to confer chemoresistance have remained poorly understood and underexplored. This comprehensive review aims to shed light on the genes linked to different chemoresistance mechanisms in OC and their intricate regulation by ncRNA and nuclear receptors. Specifically, we examine how these molecular players influence the chemoresistance mechanism. By exploring the interplay between these factors and gene expression regulation, this review seeks to provide a comprehensive mechanism driving chemoresistance in OC.

References
1.
An J, Lv W, Zhang Y . LncRNA NEAT1 contributes to paclitaxel resistance of ovarian cancer cells by regulating ZEB1 expression via miR-194. Onco Targets Ther. 2017; 10:5377-5390. PMC: 5691924. DOI: 10.2147/OTT.S147586. View

2.
Bai L, Wang A, Zhang Y, Xu X, Zhang X . Knockdown of MALAT1 enhances chemosensitivity of ovarian cancer cells to cisplatin through inhibiting the Notch1 signaling pathway. Exp Cell Res. 2018; 366(2):161-171. DOI: 10.1016/j.yexcr.2018.03.014. View

3.
Xiao S, Zhang M, Liu C, Wang D . MiR-514 attenuates proliferation and increases chemoresistance by targeting ATP binding cassette subfamily in ovarian cancer. Mol Genet Genomics. 2018; 293(5):1159-1167. DOI: 10.1007/s00438-018-1447-0. View

4.
He M, Wu H, Jiang Q, Liu Y, Han L, Yan Y . Hypoxia-inducible factor-2α directly promotes BCRP expression and mediates the resistance of ovarian cancer stem cells to adriamycin. Mol Oncol. 2018; 13(2):403-421. PMC: 6360369. DOI: 10.1002/1878-0261.12419. View

5.
Li H, Zhang W, Niu C, Lin C, Wu X, Jian Y . Nuclear orphan receptor NR2F6 confers cisplatin resistance in epithelial ovarian cancer cells by activating the Notch3 signaling pathway. Int J Cancer. 2019; 145(7):1921-1934. PMC: 6767785. DOI: 10.1002/ijc.32293. View