MicroRNA‑205 is downregulated in hepatocellular carcinoma and inhibits cell growth and metastasis via directly targeting vascular endothelial growth factor A

Abstract

MicroRNAs (miRs) are an emerging class of non-coding, endogenous and small RNA molecules that serve important functions in tumorigenesis and development. The present study investigated the expression, functions and molecular mechanism underlying miR-205 in hepatocellular carcinoma. miR-205 was downregulated in hepatocellular carcinoma tissues and cell lines. Ectopic miR-205 expression suppressed hepatocellular carcinoma cell proliferation, migration and invasion . In addition, vascular endothelial growth factor A (VEGFA) was identified as a functional downstream target of miR-205 in hepatocellular carcinoma. Furthermore, knockdown of VEGFA revealed the same functions with miR-205 overexpression in hepatocellular carcinoma cells. These results provided evidence that miR-205 served important functions in the inhibition of hepatocellular carcinoma cells growth and metastasis via directly targeting VEGFA, which indicated that miR-205 may have therapeutic value for hepatocellular carcinoma.

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

“…VEGFA mRNA expression levels negatively correlated with miR‐205‐5p expression, highlighting the transcriptional regulation of VEGFA mRNA by this miRNA. Previous studies have already identified the regulation of VEGFA by miR‐205‐5p . Additionally, the results reported here indicate that the VEGFA/miR‐205‐5p correlation might be regulated by OS in ARPE‐19 cells.…”

“…7 In addition, we have identified some potential targets of miR-205-5p and their biological processes. 7,[11][12][13]47 Moreover, it has been suggested that miR-205-5p could interact indirectly via PI3K/AKT also involved in angiogenesis. In fact, it F I G U R E 5 VEGFA-mediated Vasculogenesis is regulated by miR-205-5p.…”

“…Statistically significant differences were set at *P < .05 is well documented that miR-205-5p acts as a tumour suppressor by regulating cell migration and proliferation. 7,[11][12][13]47 Moreover, it has been suggested that miR-205-5p could interact indirectly via PI3K/AKT also involved in angiogenesis. 13 In the present report, we have observed that VEGFA and miR-205-5p are inversely expressed ( Figure 3), inducing angiogenesis.…”

<p>Propofol Inhibits Proliferation and Invasion of Stomach Cancer Cells by Regulating miR-205/YAP1 Axis</p>

“… 21 In addition, miR-205 can suppress the growth and metastasis of hepatic carcinoma cells by targeting vascular endothelial growth factor (VEGF). 22 In our study, SC cells showed weakened proliferation and invasion, intensified apoptosis, elevated caspase-3 and Bax expression, as well as lowered Bcl-2 expression after being transfected with miR-205-mimics, which indicates that miR-205 serves as a tumor suppressor in SC. We explored the association between miR-205 and propofol, finding that inhibition of miR-205 could weaken the effect of propofol on the biological events of SC cells, which suggests that propofol can act as an anticancer agent in SC by regulating miR-205.…”

11PS04 is a new chemical entity identified by microRNA-based biosensing with promising therapeutic potential against cancer stem cells

“…As expected from the expression of miR-200 family members, ZEB-1 is barely detected in epithelial cells suggesting that the downregulation of these miRs is an essential early step in tumor metastasis 20 . The EMT program itself is orchestrated by ZEB1 binding to E-boxes in the E-cadherin promoter, repressing its transcription and inciting metastatic outgrowth by causing carcinoma cells to enter a metastasis-initiating cell state 69–72 . Restoring miR-21 and miR-205 expression to non-tumorigenic levels by 11PS04 treatment also normalized the transcription and translation of PDCD4, ZEB-1 and E-Cadherin possibly altering the EMT program itself.…”