MiR-363 inhibits cisplatin chemoresistance of epithelial ovarian cancer by regulating snail-induced epithelial-mesenchymal transition

Cao, Lei; Wan, Qian; Li, Fengjie; Tang, Cui

doi:10.5483/bmbrep.2018.51.9.104

Cited by 39 publications

(34 citation statements)

References 32 publications

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“…Over-expression of miR-204-5p improves the efficacy of 5-fluorouracil in gastric cancer cells. In prostate cancer cells, miR-204-5p promotes docetaxel-mediated apoptosis [154,165] miR-206 MET Lung cancer Over-expression of miR-206 increases the anti-proliferative effects of gefitinib [158] miR-363-3p SNAI1 Ovarian cancer Silencing of miR-363-3p diminishes the anti-proliferative effects of cisplatin [166] miR-483-3p ITGB3 Lung cancer Epigenetic silencing of miR-483-3p desensitizes cells to gefitinib [154] miR-509-5p VIM, HMGA2…”

Section: Mirnas and Hgf/c-metmentioning

confidence: 99%

“…In ovarian cancer cells, miR-363-3p targets snail family transcriptional repressor 1 (SNAI1). As a consequence, the over-expression of miR-363-3p in cancer cells reverses EMT-mediated drug resistance [166]. In addition, the regulation of ZEB1 expression is mediated by miR-574-3p and miR-708-3p in gastric and breast cancer cells, respectively.…”

Section: Mirnas Directly Regulating Emt-related Transcription Factorsmentioning

confidence: 99%

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MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.Cells 2020, 9, 29 2 of 32 to confer the ability to acquire CSC properties onto cancer cells, thereby contributing to therapeutic resistance [7]. Moreover, cell-to-cell communication via extracellular vesicles among different types of cells within the cancer microenvironment could affect the efficacy of cancer therapies by delivering miRNAs that regulate various signaling pathways connected to therapeutic resistance [8,9].Combination therapies have been proposed to overcome therapeutic resistance via the combined inhibition of different mechanisms. For example, the combination of cobimetinib and pictilisib was reported to be beneficial for the treatment of colorectal cancer cells. However, resistance is unavoidable even after the combination treatment [10]. Similarly, the simultaneous inhibition of phosphoinositide 3-kinase (PI3K) and a mechanistic target of rapamycin kinase (mTOR) was reported to activate extracellular signal-regulated kinase (ERK), a pro-survival factor, in acute myeloid leukemia [11]. Therefore, it is still necessary to explore new combination strategies to defeat therapeutic resistance. An improved understanding of the cellular basis of cancer therapeutic resistance can further provide promising opportunities to design and develop novel cancer treatment strategies to manage cancers.MicroRNAs (miRNAs) are widely recognized, small, regulatory RNAs modulating numerous intracellular signaling pathways in several diseases, including cancers. Based on the expression levels and intracellular functions of miRNAs, they could act as tumor-suppressive or oncogenic factors in cancer cells [12][13][14]. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of m...

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Section: Mirnas and Hgf/c-metmentioning

confidence: 99%

Section: Mirnas Directly Regulating Emt-related Transcription Factorsmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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“…In contrast downregulation of miR-363 was observed in CIS-resistant hepatocellular carcinoma cell line [66]. Significantly lower expression level of miR-363 was also observed by Cao L. et al in CIS-resistant ovarian cancer cell line [67]. Thus, the significance of miR-363 in drug resistance can be cell line dependent.…”

Section: Discussionmentioning

confidence: 71%

The significance of microRNA genes expression in ovarian cancer cell lines resistant to cytotoxic drugs

Kaźmierczak¹,

Jopek²,

Sterzyńska³

et al. 2019

Preprint

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Ovarian cancer is the most fatal type of gynecological cancer. The main reason for high mortality is the development of drug resistance. It can be related to increased expression of drug transporters and increased expression of extracellular matrix (ECM) proteins. miRNA is a short noncoding RNA that regulates expression of about 60% of genes in the human genome and plays a crucial role in developing cancer, including resistance to chemotherapy.Our foremost aim was to exhibit alterations in the miRNA expression levels in the cisplatin (CIS), paclitaxel (PAC), doxorubicin (DOX), and topotecan (TOP) -resistant variants of W1 sensitive ovarian cancer cell line using miRNA microarray. The second goal was to identify miRNAs responsible for the regulation of drug-resistant genes.According to our observation, alterations in the expression of 40 miRNA genes. The level of expression of 21 genes was upregulated in at least one drug-resistant cell line. The expression of 19 genes was downregulated in at least one drug-resistant cell line. We identified target genes for 22 miRNAs. Target analysis showed that miRNA regulates key genes responsible for drug resistance. Among others, we observed regulation of the ABCB1 (MDR1) gene in the W1PR1 cell line by miR-363 and regulation of the COL3A1 gene in the W1TR cell line by miR-29a.Hence, on the basis of our findings, results indicate that genes responsible for drug resistance development in ovarian cancer can be regulated by miRNA.

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“…SNAIL was found to be a target of multiple miRNAs in different tumor types. SNAIL was targeted in breast cancer by miR-125b [85], miR-203 [86], miR-410-3p [87], and miR-182 [88]; in gastric cancer by miR-491-5p [89] and miR-204 [90]; in lung cancer by miR-199a [91] and miR-940 [92]; in papillary thyroid carcinoma by miR-199a [93]; in ovarian cancer by miR-137 [72] and miR-363 [94]; in hepatocellular carcinoma by miR-122 [95] and miR-502-5p [96]; in prostate cancer by miR-486-5p [97]; and in renal cancer by miR-211-5p [98]. What is more, besides tumorigenesis, SNAIL is also regulated in different processes by miRNAs.…”

Section: Micrornas Directly Targeting Snailmentioning

confidence: 99%

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

Skrzypek

Majka

2020

Cancers

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SNAIL (SNAI1) is a zinc finger transcription factor that binds to E-box sequences and regulates the expression of genes. It usually acts as a gene repressor, but it may also activate the expression of genes. SNAIL plays a key role in the regulation of epithelial to mesenchymal transition, which is the main mechanism responsible for the progression and metastasis of epithelial tumors. Nevertheless, it also regulates different processes that are responsible for tumor growth, such as the activity of cancer stem cells, the control of cell metabolism, and the regulation of differentiation. Different proteins and microRNAs may regulate the SNAIL level, and SNAIL may be an important regulator of microRNA expression as well. The interplay among SNAIL, microRNAs, long non-coding RNAs, and circular RNAs is a key event in the regulation of tumor growth and metastasis. This review for the first time discusses different types of regulation between SNAIL and non-coding RNAs with a focus on feedback loops and the role of competitive RNA. Understanding these mechanisms may help develop novel therapeutic strategies against cancer based on microRNAs.

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MiR-363 inhibits cisplatin chemoresistance of epithelial ovarian cancer by regulating snail-induced epithelial-mesenchymal transition

Cited by 39 publications

References 32 publications

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

The significance of microRNA genes expression in ovarian cancer cell lines resistant to cytotoxic drugs

Interplay among SNAIL Transcription Factor, MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Regulation of Tumor Growth and Metastasis

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