Downregulation of miR-193a-3p inhibits cell growth and migration in renal cell carcinoma by targeting PTEN

Liu, Lingqi; Li, Yanqin; Liu, Shuchao; Duan, Qixin; Chen, Liang; Wu, Teng; Qian, Huijun; Yang, Sixing; Xin, Dianqi

doi:10.1177/1010428317711951

Cited by 52 publications

(51 citation statements)

References 31 publications

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“…In human osteosarcoma, miR-142-5p also suppresses proliferation and promotes apoptosis by targeting phospholipase A and acyltransferase 3 ( 19 ). In the present study, miR-142-5p was shown to promote proliferation and migration of ccRCC cells by targeting TFAP2B , which is consistent with study results reported by Liu et al ( 20 ) that revealed that miR-142-5p promotes cell growth and migration of ccRCCs by targeting BTG anti-proliferation factor 3. These results revealed the importance of the miR-142-5p in ccRCC development.…”

Section: Discussionsupporting

confidence: 93%

miR‑142‑5p promotes renal cell tumorigenesis by targeting TFAP2B

Zhu¹,

Zou

et al. 2020

Oncol Lett

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The transcription factor AP-2 β ( TFAP2B ) serves an important role in kidney development. MicroRNAs (miRNAs) regulate carcinogenic pathways and have gained increasing attention owing to their association with human clear cell renal cell carcinoma (ccRCC) tumorigenesis. However, whether miRNAs could affect renal cell tumorigenesis by regulating TFAP2B expression has not been identified. The aim of this study was to investigate the effects of miRNA on TFAP2B and its potential role in cell growth, invasion and migration. PCR, western blot and dual luciferase reporter assays were performed to analyze the effects of miR-142-5p on TFAP2B . Furthermore, MTT, flow cytometry, wound healing and Transwell migration assays were used to analyze the effect of miR-142-5p on cell proliferation and migration. The results demonstrated that miR-142-5p targeted TFAP2B and downregulated the expression of TFAP2B at the mRNA and protein levels, promoting cell proliferation and migration in two ccRCC cell lines, 786-O and A-498. This phenomenon supported the theory that miR-142-5p may function as an oncogene in ccRCC. The potential clinical significance of miR-142-5p as a biomarker and a therapeutic target provides rationale for further investigation into miR-142-5p-mediated molecular pathways and how these may be associated with ccRCC development.

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Section: Discussionsupporting

confidence: 93%

miR‑142‑5p promotes renal cell tumorigenesis by targeting TFAP2B

Zhu¹,

Zou

et al. 2020

Oncol Lett

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“…Emerging evidences have shown that miRNAs play important roles in the development and progression of RCC [17][18][19][20][21]. These miRNAs can act as tumor suppressor genes or oncogenes by modulating the target genes.…”

Section: Discussionmentioning

confidence: 99%

MiR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway

Zhai¹,

Wu²,

Zhang³

et al. 2020

Preprint

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Backgroud: Renal cell carcinoma (RCC) is one of the most common renal malignancies in the urinary system. Numerous studies have demonstrated that miRNAs can regulate tumorigenesis and progression, while the underlying molecular mechanism for miR-6838-5p involved in RCC development is still largely unknown.Methods: The relative expression of miR-6838-5p in RCC tissues, RCC cell lines, adjacent normal tissues and normal renal epithelial cells was detected by reverse transcription polymerase chain reaction (RT-qPCR). In vitro studies, cell proliferation and invasion in human RCC cell lines ACHN and 786-O were evaluated by CCK-8 assay, Transwell assay, Colony formation assay and Flow cytometry.Bioinformatics analysis, luciferase report analysis and Western blot assay were proved that Cyclin D binding myb-like transcription factor 1 (DMTF1) is the target of miR-6838-5p.Results: Our study confirmed that miR-6838-5p was upregulated in RCC tissues (30/42, 77.43%, P < 0.01) and RCC cell lines (P < 0.05) compared to adjacent normal tissues and normal renal epithelial cells. In vitro studies demonstrated that overexpression of miR-6838-5p significantly increased cell proliferation and invasion in human RCC cell lines ACHN and 786-O (P < 0.05), whereas inhibition of miR-6838-5p inhibited cell proliferation and invasion (P < 0.05). Furthermore, we found that miR-6838-5p binds to the wild-type DMTF1 3'UTR. In addition, we found that DMTF1 was downregulation in RCC tissues and cell lines. Meanwhile, it was demonstrated in ACHN cells that overexpression of miR-6838-5p inhibited the expression of DMTF1. Finally, we also confirmed that the interaction of miR-6838-5p overexpression and DMTF1 overexpression might rescue the inhibitory effects of overexpression of miR-6838-5p on the expression of phosphatase and tensin homolog (PTEN), p53, Murine double minute 2 (MDM2) and alternative reading frame (ARF) in the DMTF1-mediated ARF-p53 downstream pathway.Conclusions: Our research shows that miR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway, which suggest that miR-6838-5pcan be used as a marker for the diagnosis of RCC.

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“…Numerous targets of miR-193a-3p have been reported [26,28,32,33]. In this study, the TargetScan, miRNA.ORG, and miRDB software were used for the prediction of target genes.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

Tian

Hong

et al. 2020

Preprint

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Abstract Background:Mitogen-inducible gene 6 (Mig-6) is a tumor suppressor gene that plays an important role in many types of cancers by interacting with EGFR. Thus far, little is known about the molecular mechanism of Mig-6 in hepatocellular carcinoma (HCC). Also, the relationship between Mig-6 and miRNAs needs to be elucidated. Therefore, this study first aimed to find whether Mig-6 could promote apoptosis and inhibition of the flux of autophagy by its downstream miRNA in HCC cell lines. Methods: Two cell lines, HepG2and HLE, were used in this study. Mig-6 overexpression and knockdown models , miR-193a mimics and inhibitors models,were established. MiRNA microarray profiling were used to verified Mig-6 regulated- miRNA. Real-time PCR, Western blot analysis were carried out to detect RNA and protein expression.Evaluation of fluorescent LC3 puncta and cell fow cytometer assay were used to test the autophagy and apoptosis respectively. Results: Mig-6 induced the apoptosis and reduced the autophagy of HCC cell lines. MiR-193a-3p is a Mig-6-regulated miRNA in Mig-6 overexpression model, and miR-193a-3p affected the apoptosis and autophagy of HCC cells by regulating the expression of TGF-β2. Additionally, the relationship between Mig-6 and transforming growth factor TGF-β2 was explored in depth for the first time.Conclusion:These findings revealed an important regulatory axis Mig-6/miR-193a-3p/TGF-β2 in the apoptosis and autophagy of HCC cells, providing a novel insight into the therapeutic target in HCC.

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Downregulation of miR-193a-3p inhibits cell growth and migration in renal cell carcinoma by targeting PTEN

Cited by 52 publications

References 31 publications

miR‑142‑5p promotes renal cell tumorigenesis by targeting TFAP2B

miR‑142‑5p promotes renal cell tumorigenesis by targeting TFAP2B

MiR-6838-5p enhances the growth and invasion of renal cell carcinoma dependent on DMTF1 via inhibiting the ARF-p53 pathway

WITHDRAWN: Mig-6 Promotes the Apoptosis and Inhibits of the Flux of Autophagy in HCC Cell Lines Through Modulating Mig-6/miR-193a-3p/TGF-β2 Axis

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