MicroRNA-122 acts as tumor suppressor by targeting TRIM29 and blocking the activity of PI3K/AKT signaling in nasopharyngeal carcinoma in vitro

Abstract

Nasopharyngeal carcinoma (NPC) is endemic in the southern provinces of China and Southeast Asia. It has been reported that microRNA-122 (miR-122) and tripartite motif-containing protein 29 (TRIM29) serve important roles in many types of tumor. The present study aimed to evaluate the expression of miR-122 and TRIM29, and their clinical significance in NPC, and to examine the associated molecular mechanisms. It was observed that low expression of miR-122 and high expression of TRIM29 led to a low overall survival rate in patients with NPC, which was associated with tumor-node-metastasis (TNM) stage and distant metastasis of NPC. Low expression of miR-122 was correlated reciprocally with high expression of TRIM29 in NPC tissues, and the two were aggravated by radiation treatment in NPC cell lines. Through Cell Counting kit-8 and Transwell assays, miR-122 was demonstrated to be able to inhibit the proliferation, migration and invasion of NPC cells. Through reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analyses, the expression of metastasis-associated genes, including E-cadherin, metastatic tumor antigen 1, matrix metalloproteinase-2 and metalloproteinase inhibitor 2 were demonstrated to be regulated by miR-122 in NPC cells. Additionally, through a luciferase assay, RT-qPCR and western blot analysis, it was demonstrated that TRIM29 may be a direct target of miR-122. In addition, it was noted that miR-122 decreased the expression of phosphorylated (p) phosphatidylinositol 3-kinase (PI3K) and p-RAC-α serine/threonine-protein kinase (AKT). Collectively, the results of the present study demonstrated that miR-122 may exert its tumor suppressive role by targeting TRIM29 and inhibiting the activity of PI3K/AKT signaling. It was indicated that miR-122 and TRIM29 may be developed as biomarkers of NPC, and possible molecular targets for the prevention of metastasis in patients with NPC.