MicroRNA‑214 suppresses the viability, migration and invasion of human colorectal carcinoma cells via targeting transglutaminase 2.

Colorectal carcinoma (CRC) is a common malignancy of the digestive tract. MicroRNA (miR)‑214 is considered a key hub that controls tumor networks; therefore, the effects of miR‑214 on CRC were examined and its target gene was investigated in this study. The expression levels of transglutaminase 2 (TGM2) and miR‑214 were detected in CRC and adjacent normal tissues by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting, and luciferase activity was analyzed by dual luciferase reporter analysis. In addition, cell viability, invasion and migration were measured by Cell Counting kit‑8 and Transwell assays, respectively. The expression levels of epithelial‑mesenchymal transition‑related proteins, and phosphoinositide‑3 kinase (PI3K)/protein kinase B (Akt) signaling‑associated factors were detected using RT‑qPCR and western blotting. The results demonstrated that miR‑214 expression was downregulated in CRC tissue, whereas TGM2 expression was upregulated. According to TargetScan prediction, miR‑214 possesses a binding site to TGM2. In addition, transfection with miR‑214 mimics markedly suppressed the viability of LoVo cells. miR‑214 overexpression also inhibited cell invasion and migration by increasing E‑cadherin and tissue inhibitor of metalloproteinases‑2 expression, and decreasing matrix metalloproteinase (MMP)‑2 and MMP‑9 expression. Furthermore, miR‑214 downregulated phosphorylation of PI3K and Akt; however, the expression levels of total PI3K and Akt were not affected by miR‑214. In conclusion, this study indicated that TGM2 was a target gene of miR‑214, and a negative correlation between miR‑214 and TGM2 expression was determined in CRC. Notably, miR‑214 markedly suppressed the viability, invasion and migration of CRC cells, which may be associated with a downregulation in PI3K/Akt signaling. These findings suggested that miR‑214 may be considered a novel target for the treatment of CRC.