MicroRNA-32 (miR-32) regulates phosphatase and tensin homologue (PTEN) expression and promotes growth, migration, and invasion in colorectal carcinoma cells

Abstract

BackgroundColorectal carcinoma (CRC) is one of the leading causes of cancer-related mortality worldwide. MicroRNAs (miRNAs, miRs) play important roles in carcinogenesis. MiR-32 has been shown to be upregulated in CRC. In this study, we identified the potential effects of miR-32 on some important biological properties of CRC cells, and clarified the regulation of PTEN by miR-32.MethodsThe effect of miR-32 on PTEN expression was assessed in CRC cell lines with miR-32 mimics/inhibitor to increase/decrease miR-32 expression. Furthermore, the roles of miR-32 in regulating CRC cells biological properties were analyzed with miR-32 mimics/inhibitor-transfected cells. The 3′-untranslated region (3′-UTR) of PTEN combined with miR-32 was verified by dual-luciferase reporter assay.ResultsGain-of-function and loss-of-function studies showed that overexpression of miR-32 promoted SW480 cell proliferation, migration, and invasion, reduced apoptosis, and resulted in downregulation of PTEN at a posttranscriptional level. However, miR-32 knock-down inhibited these processes in HCT-116 cells and enhanced the expression of PTEN protein. In addition, we further identified PTEN as the functional downstream target of miR-32 by directly targeting the 3′-UTR of PTEN.ConclusionsOur results demonstrated that miR-32 was involved in tumorigenesis of CRC at least in part by suppression of PTEN.

miR‑20b promotes cellular proliferation and migration by directly regulating phosphatase and tensin homolog in prostate cancer

“…PTEN functions as a negative regulator of the phosphoinositide 3-kinase/Akt pathway through dephosphorylation of phosphatidylinositol 3,4,5 trisphosphate, and is involved in regulation of cellular proliferation, metastasis and apoptosis during progression of cancers (34). PTEN has been reported to be regulated by numerous miRNAs in multiple cancers, including colorectal carcinoma, glioma, ovarian and breast cancer (29,(35)(36)(37). In the present study, it was also determined that miR-20b inhibited PTEN expression by directly binding to the mRNA 3'-UTR of PTEN in VCaP and PC-3 cells.…”

Downregulation of HNF1 homeobox B is associated with drug resistance in ovarian cancer

“…Similarly, miR-375 is associated with drug resistance in ovarian (71) and cervical cancer (72). Although no study has reported the role of miR-32 and -217 in drug resistance, it is associated with drug resistance-related processes such as cell proliferation, invasion and migration (73)(74)(75). Collectively, among the 7 microRNAs most strongly targeting HNF1B, the majority were involved in drug resistance in ovarian and other types of cancers, suggesting that the gene also mediates drug resistance.…”

The Current Screening Technologies of Gene Expression Profile in Diabetes Mellitus

“…A complicated metabolic disorder such as diabetes is affected by broad gene expression in numerous tissues. A recent study has reported that six candidate genes were found significantly high in the T2DM study; ENND1B, LYN, MRPL30, POC1B, PRKCB, and RP4-655J12.3 [28]. PRKCB is observed to be upregulated in skeletal muscle, islets, adipose tissue, and blood, and downregulated in the liver of T2DM subject, suggested to involve in IR and decreased β-cell function.…”

“…It is a complex endocrine and metabolic disorder with various of complications rises, characterized by IR and deficient β-cell function [28]. The pathogenesis of the disease is suggested to be affected by the intercommunication of multiple genetics and risk factors.…”

“…Contrarily, SREBP1 and lipogenic target genes were upregulated indicating increased in fatty acid biosynthesis that leads to increasing fatty acid production from the liver. Other than that, a study has proposed eight candidates gene for obesity; BAP1, GRB14, HSP90AB1, ITGA5, NCKAP5L, SP1, and TOMM5; closely related with PRKCB and LYN, the candidate genes of T2DM [28].…”