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

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.