Effects of Sam68 gene silencing on proliferation of nasopharyngeal carcinoma cell line 5-8F and its possible molecular mechanism.
- Author:
Bin YANG
1
;
Dehui FENG
Author Information
- Publication Type:Journal Article
- MeSH: Adaptor Proteins, Signal Transducing; genetics; metabolism; Carcinoma; Cell Line, Tumor; Cell Proliferation; DNA-Binding Proteins; genetics; metabolism; Forkhead Box Protein O3; Forkhead Transcription Factors; metabolism; Gene Silencing; Glycogen Synthase Kinase 3; metabolism; Glycogen Synthase Kinase 3 beta; Humans; Nasopharyngeal Neoplasms; genetics; pathology; Proto-Oncogene Proteins c-akt; metabolism; RNA, Messenger; genetics; metabolism; RNA, Small Interfering; genetics; RNA-Binding Proteins; genetics; metabolism
- From: Journal of Southern Medical University 2013;33(2):258-261
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of Sam68 gene silencing on proliferation of nasopharyngeal carcinoma (NPC) cell line 5-8F and explore its possible molecular mechanism.
METHODSThe NPC cell line 5-8F was transfected with a small interfering RNA (siRNA) targeting Sam68 and the cell proliferation changes were observed. Quantitative RT-PCR and Western blotting were used to examine the changes in the expressions of Sam68, cell cycle-related proteins, and some up-stream proteins in the transfected cells.
RESULTSTransfection of 5-8F cells with Sam68-specific siRNA significantly lowered the mRNA and proteins levels of Sam68, suppressed cell proliferation, decreased the expression of Cyclin D1, and increased the expression of p27. The transfected cells showed obviously decreased expressions of p-FOXO3a, p-Akt and p-GSK-3β, but the expressions of FOXO3a, Akt and GSK-3β were not obviously affected.
CONCLUSIONSSam68 modulates the proliferation of NPC cells probably by activating Akt/FOXO3a pathway and regulating the cell proliferation-related molecules.
