Down-regulation of miR-155 promotes apoptosis of nasopharyngeal carcinoma CNE-1 cells by targeting PI3K/AKT-FOXO3a signaling

S. Wu, D.-L. Xie, X.-Y. Dai

Department of E.N.T. & H.N, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province, China. wush68@sysu.edu.cn

---

• Oncology

OBJECTIVE: Nasopharyngeal carcinoma is one of the common malignant tumors of the ear, nose, and throat in China. Cell apoptosis is expected to be closely related to prognosis. In recent years, with the development of non-coding RNA function research, it is proposed that miRNA plays an important role in the pathogenesis of nasopharyngeal carcinoma. This study aimed to investigate the role of miR-155 in the apoptosis of nasopharyngeal carcinoma cells.

PATIENTS AND METHODS: Cell transfection was performed to knockdown or overexpress the level of miR-155 or knockdown of the level of FOXO3a. The expression of the related protein was detected by immunoblotting. The Real Time quantitative-PCR was used to detect miR-155 expression. Cell proliferation was assessed by MTT assay. The changes of cell apoptosis were observed by flow cytometry using AV-PI staining and TUNEL staining.

RESULTS: The miR-155 inhibitor and mimics were successfully capable of knocking down or overexpressing miR-155 levels. After knocking down miR-155 level, cell proliferation was significantly attenuated, and apoptosis was significantly increased compared with the sham group (p < 0.05). After overexpression of miR-155, opposite results were observed. In addition, in the cells with the knockdown of miR-155 level, further knockdown of FOXO3a level significantly reduced the inhibitory effect of miR-155 on cell apoptosis compared with the control group (p < 0.05).

CONCLUSIONS: In nasopharyngeal carcinoma CNE-1 cell line, miR-155 can inhibit the proliferation and promote apoptosis of nasopharyngeal carcinoma cells by targeting PI3K/AKT-FOXO3a signaling. MiR-155 may be a novel target for the treatment of nasopharyngeal carcinoma.

Free PDF Download