MiR-155 promotes proliferation and inhibits apoptosis of nasopharyngeal carcinoma cells through targeting PTEN-PI3K/AKT pathway

W.-N. Zuo, H. Zhu, L.-P. Li, A.-Y. Jin, H.-Q. Wang

Department of Otorhinolaryngology, Cangzhou Central Hospital, Cangzhou, Hebei, China. shuo93970366@yeah.net

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• Oncology

OBJECTIVE: Nasopharyngeal carcinoma (NPC) is a polygenic hereditary disease, and the exact pathogenesis remains poorly understood. MiR-155 regulates the development and progression of several tumors. However, the role of MiR-155 in NPC has not been elucidated.
PATIENTS AND METHODS: The NPC cell line CNE2 was cultured in vitro and divided into control group, miR-155 mimics group, and miR-155 inhibitor group, followed by analysis of miR-155 expression by real-time PCR, cell proliferation by MTT assay, cell invasion by transwell chamber, Caspase3 activity, apoptosis of CNE2 cells by flow cytometry, and the expression of PTEN-PI3K/AKT signaling pathway by Western blot.
RESULTS: Transfection of miR-155 mimics significantly up-regulated miR-155 expression, promoted the proliferation and invasion of CNE2 cells, inhibited Caspase 3 activity, and decreased cell apoptosis, and PTEN expression, as well as increased PI3K/AKT phosphorylation, compared with control group (p < 0.05). Transfection of miR-155 inhibitor inhibited the proliferation and invasion of CNE2 cells, increased Caspase 3 activity, cell apoptosis, and PTEN expression, as well as reduced PI3K/AKT phosphorylation. Compared with control group, the differences were statistically significant (p < 0.05).
CONCLUSIONS: Up-regulation of miR-155 can promote the proliferation of NPC cells and inhibit cell apoptosis by targeting the PTEN-PI3K/AKT pathway, thereby participating in the development and invasion of NPC, indicating that it might be a potential novel target for treating NPC.

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