Overexpression of Long Noncoding RNA E2F-Mediated Cell Proliferation Enhancing Long Noncoding RNA Is Involved in the Development of Chemoresistance of Cancer Cells to Carboplatin in Ovarian Endometrioid Adenocarcinoma

Zhao, Lei; Yang, Jing; Liu, Xinlian; Xi, Fu; Ding, Yan; Wang, Chunyan

doi:10.1089/cbr.2019.2851

Cited by 6 publications

(7 citation statements)

References 22 publications

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“…Carboplatin is a widely used chemotherapeutic drug for EOC, but the development of carboplatin resistance substantially limits the treatment effect of chemotherapy. A growing number of studies have proven that lncRNA dysregulation is a possible reason for chemoresistance in different human cancers, including EOC 15 16 . Identification of novel EOC-specific chemoresistance-associated lncRNAs is important for the future identification of lncRNA-targeted treatment.…”

Section: Discussionmentioning

confidence: 99%

LncRNA-H19 regulates chemoresistance to carboplatin in epithelial ovarian cancer through microRNA-29b-3p and STAT3

et al. 2021

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Background: Platinum-based chemotherapy is part of current standard treatment for epithelial ovarian cancer (EOC). However, chemoresistance often rapidly developed, leading to chemotherapy failure and unfavored prognosis. Increasing evidence has demonstrated the important role of oncogenic long noncoding RNA H19 in various cancers, including EOC. No current study is available in exploring the role of lncRNA-H19 in carboplatin resistance of EOC and its underlying mechanism. Methods: Levels of lncRNA-H19, miR-29b-3p, and STAT3 mRNA were measured by qRT-PCR. The 50% inhibitory concentration value was detected with Cell Counting Kit-8 (CCK8). Colony-formation and CCK8 assays were employed to measure cell viability. Cell migration and invasion ability was evaluated with transwells. Western blot assay was utilized to measure P-gp, MRP1, LRP, and STAT3 protein levels. The targeting between lncRNA-H19 and miR-29b-3p, as well as miR-29b-3p and STAT3, was verified by dual-luciferase, RNA immunoprecipitation, and RNA pull-down experiments. Results: lncRNA-H19 and STAT3 were sharply increased, while miR-29b-3p was decreased in carboplatin-resistant EOC. Carboplatin efficacy was enhanced by lncRNA-H19 silencing in chemo-resistant EOC cells. lncRNA-H19 served as a competing endogenous RNA of miR-29b-3p, causing the derepression of miR-29b-3p downstream target STAT3, leading to chemoresistance in carboplatin-tolerated EOC. Conclusions: The lncRNA-H19/miR-29b-3p axis improved carboplatin resistance of EOC by targeting STAT3, indicating a possible approach to improving chemotherapy for EOC.

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Section: Discussionmentioning

confidence: 99%

LncRNA-H19 regulates chemoresistance to carboplatin in epithelial ovarian cancer through microRNA-29b-3p and STAT3

et al. 2021

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“…SNHG22 sponges miR-2467 to enhance Gal-1 expression, and Gal-1 activates the H-Ras/Raf/ERK pathway to induce apoptosis inhibition and drug resistance ( 58 ). Likewise, lncRNA EPEI upregulation indirectly downregulates P53 expression, leading to carboplatin resistance in ovarian endometrioid adenocarcinoma ( 59 ). Inactivation of P53, a tumor suppressor gene, can promote carcinogenesis and inhibit cell apoptosis ( 60 ).…”

Section: Ectopic Expression Of Lncrnas Mediates Chemotherapeutic Resistancementioning

confidence: 99%

The Non-Coding RNAs Inducing Drug Resistance in Ovarian Cancer: A New Perspective for Understanding Drug Resistance

Gong

Cao

et al. 2021

Front. Oncol.

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Ovarian cancer, a common malignant tumor, is one of the primary causes of cancer-related deaths in women. Systemic chemotherapy with platinum-based compounds or taxanes is the first-line treatment for ovarian cancer. However, resistance to these chemotherapeutic drugs worsens the prognosis. The underlying mechanism of chemotherapeutic resistance in ovarian cancer remains unclear. Non-coding RNAs, including long non-coding RNAs, microRNAs, and circular RNAs, have been implicated in the development of drug resistance. Abnormally expressed non-coding RNAs can promote ovarian cancer resistance by inducing apoptosis inhibition, protective autophagy, abnormal tumor cell proliferation, epithelial-mesenchymal transition, abnormal glycolysis, drug efflux, and cancer cell stemness. This review summarizes the role of non-coding RNAs in the development of chemotherapeutic resistance in ovarian cancer, including their mechanisms, targets, and potential signaling pathways. This will facilitate the development of novel chemotherapeutic agents that can target these non-coding RNAs and improve ovarian cancer treatment.

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“…E2F-mediated cell proliferation enhancing lncRNA (EPEL) was originally identified in lung cancer [ 110 ]. Zhao et al reported that the plasma level of EPEL is elevated in endometrioid adenocarcinoma patients compared to healthy patients [ 59 ]. Mechanistically, the overexpression of EPEL markedly dampened the expression of p53, thereby conferring carboplatin resistance.…”

Section: Lncrnas and Chemoresistance In Ovarian Cancermentioning

confidence: 99%

“…Mechanistically, the overexpression of EPEL markedly dampened the expression of p53, thereby conferring carboplatin resistance. Additionally, p53 overexpression did not alter EPEL expression level, suggesting that EPEL is an upstream inhibitor of p53 [ 59 ]. In a similar way, a study has been conducted to determine the effect of the carboplatin/docetaxel combination on the expression levels of several lncRNAs in an OC cell line, 3AO [ 60 ].…”

Section: Lncrnas and Chemoresistance In Ovarian Cancermentioning

confidence: 99%

Back to the Future: Rethinking the Great Potential of lncRNAS for Optimizing Chemotherapeutic Response in Ovarian Cancer

Elsayed

Amero

Salama

et al. 2020

Cancers

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Ovarian cancer (OC) is one of the most fatal cancers in women worldwide. Currently, platinum- and taxane-based chemotherapy is the mainstay for the treatment of OC. Yet, the emergence of chemoresistance results in therapeutic failure and significant relapse despite a consistent rate of primary response. Emerging evidence substantiates the potential role of lncRNAs in determining the response to standard chemotherapy in OC. The objective of this narrative review is to provide an integrated, synthesized overview of the current state of knowledge regarding the role of lncRNAs in the emergence of resistance to platinum- and taxane-based chemotherapy in OC. In addition, we sought to develop conceptual frameworks for harnessing the therapeutic potential of lncRNAs in strategies aimed at enhancing the chemotherapy response of OC. Furthermore, we offered significant new perspectives and insights on the interplay between lncRNAs and the molecular circuitries implicated in chemoresistance to determine their impacts on therapeutic response. Although this review summarizes robust data concerning the involvement of lncRNAs in the emergence of acquired resistance to platinum- and taxane-based chemotherapy in OC, effective approaches for translating these lncRNAs into clinical practice warrant further investigation.

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Overexpression of Long Noncoding RNA E2F-Mediated Cell Proliferation Enhancing Long Noncoding RNA Is Involved in the Development of Chemoresistance of Cancer Cells to Carboplatin in Ovarian Endometrioid Adenocarcinoma

Cited by 6 publications

References 22 publications

LncRNA-H19 regulates chemoresistance to carboplatin in epithelial ovarian cancer through microRNA-29b-3p and STAT3

LncRNA-H19 regulates chemoresistance to carboplatin in epithelial ovarian cancer through microRNA-29b-3p and STAT3

The Non-Coding RNAs Inducing Drug Resistance in Ovarian Cancer: A New Perspective for Understanding Drug Resistance

Back to the Future: Rethinking the Great Potential of lncRNAS for Optimizing Chemotherapeutic Response in Ovarian Cancer

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