Small interfering RNA-mediated RIP1 knockdown enhances L-OHP sensitivity of human oral squamous carcinoma cells.
- Author:
Jincheng XU
1
;
Yingying HUANG
;
Yang LI
;
Longjian PU
;
Fei XIA
;
Chenchen JIANG
;
Hao LIU
;
Zhiwen JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Carcinoma, Squamous Cell; genetics; pathology; Cell Line, Tumor; Gene Expression Regulation, Neoplastic; Humans; Mouth Neoplasms; genetics; pathology; Organoplatinum Compounds; pharmacology; RNA Interference; RNA, Small Interfering; genetics; Receptor-Interacting Protein Serine-Threonine Kinases; genetics; Transfection
- From: Journal of Southern Medical University 2013;33(7):1004-1007
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of small interfering RNA-mediated receptor-interacting protein kinase 1 (RIP1) knockdown on the sensitivity of human oral squamous carcinoma cells to to oxaliplatin (L-OHP)-induced apoptosis and explore a new target for clinical treatment of oral squamous carcinoma.
METHODSThe viability of human oral squamous carcinoma cell line KB exposed to different concentrations (0, 0.25, 0.5, 1, 2, 4 µmol/L) of L-OHP were detected by MTT assay. PI/Annexin V staining was used to observe cell apoptosis in naive KB cells, cell and transfected with pSH1Si-RIP1 or with the empty plasmid. Western blotting was used to detect RIP1 expression in KB cells exposed to L-OHP and in cells transfected with pSH1Si-RIP1.
RESULTSExposure to L-OHP (1µmol/L) for 24, 48, 72 h resulted in KB cell survival rates of 67.66%, 55.17%, and 41.34%, respectively, but the cell apoptosis rate was only 9.6% following a 24-h exposure. KB cells transfected with pSH1Si-RIP1 showed an apoptotic rate of 9.4%, which increased to 29.1% following L-OHP exposure. RIP1 expression was first up-regulated and then down-regulated in KB cells treated with L-OHP, and was significantly reduced after cell transfection with pSH1Si-RIP1.
CONCLUSIONSuppression of RIP1 expression increases the apoptotic rate of human oral squamous carcinoma cells, suggesting the potential of RIP1 as a new candidate target for clinical treatment of oral squamous carcinoma.
