MicroRNA-152 Targets Phosphatase and Tensin Homolog to Inhibit Apoptosis and Promote Cell Migration of Nasopharyngeal Carcinoma Cells
Shunde Huang, Xiaohua Li, Haotu Zhu
ENT & HN Surgery Department, Zhengzhou Central Hospital affiliated with Zhengzhou University, Zhengzhou, Henan, China (mainland)
Med Sci Monit 2016; 22:4330-4337
Available online: 2016-11-13
Nasopharyngeal carcinoma (NPC) is a type of head and neck cancer with very high prevalence in southern China. Phosphatase and tensin homolog (PTEN), a tumor suppressor, was reported to be downregulated in NPC patients and correlated with pathological grade and clinical stage of NPC.
MATERIAL AND METHODS: Luciferase reporter assay, qPCR, and Western blot analysis were used to determine if PTEN is a target of miR-152. The function of miR-152 in cell apoptosis and cell proliferation was examined as well. Tissue samples from NPC patients were also analyzed for PTEN and miR-152 expressions.
RESULTS: Reporter assay indicated miR-152 targets the 3’UTR of PTEN mRNA to inhibit PTEN expression. Transfection of the NPC-derived cell line with miR-152 mimic confirmed these findings. Overexpression of miRNA-152 inhibits apoptosis induced by Cisplatin in NPC cancer cells in vitro. Moreover, overexpression miR-152 also promotes NPC cancer cell invasion and proliferation. Samples from EBV-negative NPC patients demonstrated the down-regulated level of PTEN may be related with overexpression of miR-152.
CONCLUSIONS: The miR-152 targets PETN to inhibit cell apoptosis and promote cancer cell proliferation and migration in NPC development.
Keywords: Apoptosis - genetics, 3' Untranslated Regions, Cell Line, Tumor, Cell Movement - genetics, Cell Proliferation - genetics, Cisplatin - pharmacology, Down-Regulation, MicroRNAs - metabolism, Nasopharyngeal Neoplasms - pathology, PTEN Phosphohydrolase - metabolism, Proto-Oncogene Proteins c-akt - metabolism, RNA, Messenger - metabolism