4.6 Article

miR-9-5p facilitates hepatocellular carcinoma cell proliferation, migration and invasion by targeting ESR1

期刊

MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 476, 期 2, 页码 575-583

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SPRINGER
DOI: 10.1007/s11010-020-03927-z

关键词

miR-9-5p; ESR1; Hepatocellular carcinoma; Proliferation; Migration; Invasion

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The study revealed that miR-9-5p is highly expressed in HCC cells while ESR1 is poorly expressed; overexpression of miR-9-5p can enhance cell proliferation, invasion, and migration; ESR1 is identified as a downstream target of miR-9-5p in HCC.
The study aimed to explore the relationship between miR-9-5p and ESR1, and clarify the underlying functional mechanism in the occurrence and development of hepatocellular carcinoma (HCC). Expression data including miRNAs and mRNAs of HCC downloaded from TCGA database were processed for differential analysis, and corresponding clinical data were collected for survival analysis to identify the target miRNA miR-9-5p. Bioinformatics databases were applied for predicting downstream target mRNAs of miR-9-5p. qRT-PCR was used to evaluate expression of miR-9-5p. Western blot was used to detect protein expression of ESR1. MTT, wound healing assay and Transwell assay were used to detect HCC cell proliferation, migration and invasion, respectively. Dual-luciferase reporter gene assay was used to identify the targeting relationship between miR-9-5p and ESR1. Research suggested that miR-9-5p was highly expressed in HCC cells but ESR1 was poorly expressed. Overexpression of miR-9-5p could improve the proliferation, invasion and migration of cells. Dual-luciferase reporter assay showed that ESR1 was the downstream target of miR-9-5p in HCC. Overexpression of miR-9-5p markedly reduced ESR1 mRNA and protein levels in HCC cells, whereas inhibition of miR-9-5p expression produced the contrary results. Silencing ESR1 could noticeably reverse the effect of miR-9-5p knockdown on the proliferation, migration and invasion of HCC cells. As an oncogene, miR-9-5p fostered the proliferation, migration and invasion of HCC cells by targeting and inhibiting ESR1 expression.

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