Role of STAT3-Interacting Protein (STIP1) in delta12-Prostaglandin J2-Induced Cell Death.
- Author:
Seong Mook KIM
1
;
Sun LEE
;
Hwan Jong KWAK
;
Bo Eun KIM
;
Dong Jin KIM
;
In Kyung KIM
;
Seong Whan JEONG
Author Information
1. Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Korea. swjeong@cmc.cuk.ac.kr
- Publication Type:Original Article
- Keywords:
delta12-Prostaglandin J2;
STAT3-interacting protein;
STAT3, Apoptosis;
Bax
- MeSH:
Apoptosis;
Carcinogenesis;
Cell Death*;
DNA, Complementary;
Genistein;
Prostaglandins;
Protein Kinases
- From:The Korean Journal of Physiology and Pharmacology
2004;8(1):27-31
- CountryRepublic of Korea
- Language:English
-
Abstract:
delta12-Prostaglandin J2 (delta12-PGJ2) is one of cyclopentenone prostaglandins. The delta12-PGJ2 is known to induce apoptosis of tumor cells, however, it's action mechanism is not clear. It has recently been reported that STAT3 is involved in tumorigenesis. In the present study, we investigated the role of STAT3-interacting protein (STIP1) in the cytotoxicity of delta12-PGJ2, since STIP1 was recently reported as a modulator of STAT3 activation by specifically binding to inactive (unphosphorylated) STAT3. The effect of delta12-PGJ2 was observed in stably overexpressing Neuro-2A cells transfected with full cDNA of STIP1, and cytotoxicity of delta12-PGJ2 in the transfected cells was increased, compared with the vector control cells. The cytotoxicity of delta12-PGJ2 treatment was significantly accentuated by pretreatment of the STIP1-transfected cells with protein kinase inhibitor, genistein, and less activation of STAT3 in STIP1-transfected cells was shown, compared with the vector control cells. Expression of bax was also increased in the STIP1-transfected cells. These data suggest that STIP1 inhibits cell growth via inhibition of STAT3 activation in delta12-PGJ2 treatment.
