Reconstructing the JAK/STATs signal pathway restored the anti-proliferative response of MHCC97 on interferon alpha.
- Author:
Wei-zhong WU
1
;
Hui-chuan SUN
;
Yan-qin GAO
;
Lu WANG
;
Zhao-you TANG
;
Kang-da LIU
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Hepatocellular; genetics; metabolism; pathology; Cell Line, Tumor; Cell Proliferation; Humans; Interferon-Stimulated Gene Factor 3, gamma Subunit; genetics; Interferon-alpha; metabolism; pharmacology; Janus Kinases; genetics; physiology; Liver Neoplasms; genetics; metabolism; pathology; STAT Transcription Factors; genetics; physiology; Signal Transduction; Transfection
- From: Chinese Journal of Hepatology 2006;14(4):277-280
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo elucidate the roles of JAK/STATs signal pathway on anti-proliferative effects induced by IFN-alpha in MHCC97.
METHODSAn IRF9 expression vector was transfected into MHCC97 with Dosper. The expression of IRF9, cycle regulating proteins and the forming of ISGF3 complex were detected using Western blot and EMSA, respectively. Cell proliferation and distribution were monitored using MTT and flow cytometry.
RESULTSHigh expression of IRF9 restored the anti-proliferative response of MHCC97 on IFN-alpha treatment and delayed the cell transition from S phase to G2 phase induced by IFN-alpha.
CONCLUSIONThe integrity and functions of JAK/STATs signal pathway played an important role in mediating the anti-proliferative effects of IFN-alpha in MHCC97.
