miR-93 Promotes Cell Proliferation in Gliomas through Activation of PI3K/Akt Signaling Pathway

Jiang, Lili; Wang, Chanjuan; Lei, Fangyong; Zhang, Longjuan; Zhang, Xin; Liu, Aibin; Wu, Geyan; Zhu, Jinrong; Song, Libing

doi:10.18632/oncotarget.3221

Cited by 101 publications

(89 citation statements)

References 59 publications

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“…Similarly, in breast cancers, miR-93 has been found to decrease multiple carcinogenic processes, interestingly, in an Nrf2-dependent manner [23]. On the other hand, in some malignancies, such as gastric cancer, hepatocellular carcinoma, non-small-cell lung cancer, osteosarcoma, ovarian cancer, and gliomas, miR-93 down-regulates tumour suppressor (mostly PTEN) expression and has consequently been linked to more aggressive cancer phenotypes in both experimental and clinical studies [38-43]. …”

Section: Discussionmentioning

confidence: 99%

Expression Levels of microRNAs miR-93 and miR-200a in Pancreatic Adenocarcinoma with Special Reference to Differentiation and Relapse-Free Survival

et al. 2018

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Objectives: Protein levels of the transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2) and its inhibitor Kelch-like ECH-associated protein 1 (Keap1) have been proposed as prognostic factors in pancreatic ductal adenocarcinomas (PDACs). These cellular redox-state-regulating enzymes are targeted by several microRNAs, including miR-93 and miR-200a. Methods: We assessed mRNA levels of Nrf2 and Keap1 and tissue expression of miR-93 and miR-200a in 51 patients with surgically treated PDAC. Expression levels were separately measured in malignant cells and adjacent benign cells. Results: Keap1 and Nrf2 mRNA expression levels in cancer cells were lower than in adjacent benign tissue (Wilcoxon’s test; p = 0.0015 and p = 0.000032, respectively). Conversely, miR-93 expression was higher in cancer cells than in adjacent benign tissue (p = 0.00082). Low levels of miR-93 and miR-200a in cancer cells were associated with poorer differentiation (p = 0.004 and p = 0.002, respectively). In univariate survival analysis, benign-tissue levels of miR-200a above the median predicted better relapse-free survival (RFS) (p = 0.045). Conclusions: High miR-93 and miR-200a levels in cancer cells of PDAC were associated with better differentiation, and miR-200a expression in benign tissue with excellent RFS. Keap1 and Nrf2 mRNA levels showed prominent down-regulation in cancerous versus benign tissue, but they were not associated with disease aggressiveness or outcome.

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Section: Discussionmentioning

confidence: 99%

Expression Levels of microRNAs miR-93 and miR-200a in Pancreatic Adenocarcinoma with Special Reference to Differentiation and Relapse-Free Survival

et al. 2018

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“…In recent years, miR-93 has been found to be deregulated and to generally have a promoting role in certain human cancer types (23,24).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-93 promotes cell proliferation by directly targeting P21 in osteosarcoma cells

2017

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRNAs) are small, non-coding RNAs that are key regulators of gene expression by directly binding to the 3'-untranslated region of their target mRNAs, resulting in translational repression or degradation of mRNA. It has been demonstrated that miRNAs have key roles in a variety of human malignancies, including osteosarcoma. The present study aimed to assess the molecular mechanism of miR-93 in the regulation of osteosarcoma cell proliferation. Reverse-transcription quantitative PCR and western blot assays were used to examine mRNA and protein expression. An MTT assay and flow cytometry were performed to determine the cell proliferation and cell cycle distribution. A luciferase reporter assay was performed to confirm the direct targeting of cyclin-dependent kinase inhibitor 1A (CDKN1A), also known as P21, by miR-93, which was suggested by a bioinformatics analysis. The results showed that the expression of miR-93 was frequently and significantly increased in a total of 19 osteosarcoma tissues compared to their matched adjacent non-tumor tissues, and the upregulation of miR-93 was associated with the malignant progression of osteosarcoma. Furthermore, miR-93 was also upregulated in the human osteosarcoma cell lines Saos-2, U2OS, SW1353 and MG63 when compared with that in the human osteoblast cell line hFOB1.19. Transfection with miR-93 inhibitor significantly reduced the miR-93 levels and inhibited the proliferation of U2OS and MG63 osteosarcoma cells. The protein levels of P21 were negatively regulated by miR-93 in U2OS and MG63 cells. Knockdown of miR-93 caused cell cycle arrest at G1 stage in U2OS and MG63 cells, identical to the effect of P21 overexpression. Finally, P21 was found to be significantly downregulated in osteosarcoma tissues compared to their matched adjacent non-tumor tissues, suggesting that the inhibition of P21 may be due to increased miR-93 expression in osteosarcoma tissues. In conclusion, the present study demonstrated that miR-93 enhances the proliferation of osteosarcoma cells, at least in part via inhibiting P21 expression and thus promoting cell cycle progression.

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“…Although a few studies have shown that miR-93 may functionally interact with PTEN, this has only been reported in cardiomyocyte apoptosis, osteosarcoma, ovarian cancer, glioma, hepatocellular carcinoma and prostate cancer (14)(15)(16)(17)(18)(19)(20). Therefore, it remains to be determined whether miR-93 is also functionally associated with PTEN in breast cancer, and whether such an association contributes to the induction of EMT and drug resistance in breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer

Chu

Xia

et al. 2017

Oncology Reports

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Abstract. It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN.

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miR-93 Promotes Cell Proliferation in Gliomas through Activation of PI3K/Akt Signaling Pathway

Cited by 101 publications

References 59 publications

Expression Levels of microRNAs miR-93 and miR-200a in Pancreatic Adenocarcinoma with Special Reference to Differentiation and Relapse-Free Survival

Expression Levels of microRNAs miR-93 and miR-200a in Pancreatic Adenocarcinoma with Special Reference to Differentiation and Relapse-Free Survival

MicroRNA-93 promotes cell proliferation by directly targeting P21 in osteosarcoma cells

miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer

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