Downregulated miR-495-3p in colorectal cancer targets TGFβR1, TGFβR2, SMAD4 and BUB1 genes and induces cell cycle arrest.

Background: Hsa-miR-495 (miR-495) has been extensively investigated in cancer initiation and progression. On the other hand, our bioinformatics analysis suggested that miR-495 exerts its effects through targeting of TGFβ signaling components.

Methods & Results: In order to investigate such an effect, miR-495 precursor was overexpressed in HEK293T, SW480, and HCT116 cells, which was followed by downregulation of TGFβR1, TGFβR2, SMAD4, and BUB1 putative target genes, detected by RT-qPCR.

A novel miRNA located in the GATA4 gene regulates the expression of IGF-1R and AKT1/2 genes and controls cell proliferation.

GATA4 gene is a zinc-finger transcription factor known to be involved in cardiogenesis and the progression of different cancer types. Its diverse functions might be attributed to noncoding RNAs that could be embedded within its sequence. Here, we predicted a stable RNA stem-loop structure that is located in the second intron of the GATA4 gene.

Hsa-miR-587 Regulates TGFβ/SMAD Signaling and Promotes Cell Cycle Progression.

Objective: Transforming growth factor beta/single mothers against decapentaplegic (TGFβ/SMAD) signaling pathway plays important roles in various biological processes. It acts as a tumor suppressor during the early stages of cancer progression. Discovering the regulators of this pathway provides important options for therapeutic strategies.

Hsa-miR-6165 downregulates insulin-like growth factor-1 receptor (IGF-1R) expression and enhances apoptosis in SW480 cells.

MicroRNAs are small non-coding RNAs that are implicated in various biological processes. Hsa-miR-6165 (miR-6165), located in the p75NTR gene, is known to induce apoptosis in human cell lines, but its mechanism of action is not fully understood yet. Here, we predicted the insulin-like growth factor 1 receptor (IGF-1R) gene as a bona fide target for miR-6165.