Role of STAT3-Interacting Protein (STIP1) in Δ12-Prostaglandin J2-Induced Cell Death

• 영문명: Role of STAT3-Interacting Protein (STIP1) in Δ¹²-Prostaglandin J₂-Induced Cell Death
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Seong-Mook Kim Sun Lee Hwan-Jong Kwak Bo-Eun Kim Dong-Jin Kim In-Kyung
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제8권 제1호, 27~31쪽, 전체 5쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2004.01.01

영문 초록

Δ¹²-Prostaglandin J₂ (Δ¹²-PGJ₂) is one of cyclopentenone prostaglandins. The Δ ¹²-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 Δ ¹²-PGJ₂, since STIP1 was recently reported as a modulator of STAT3 activation by specifically binding to inactive (unphosphorylated) STAT3. The effect of Δ¹²-PGJ₂ was observed in stably overexpressing Neuro-2A cells transfected with full cDNA of STIP1, and cytotoxicity of Δ ¹²-PGJ₂ in the transfected cells was increased, compared with the vector control cells. The cytotoxicity of Δ¹²-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 Δ¹²-PGJ₂ treatment.

키워드

Δ¹²-Prostaglandin J₂ STAT3-interacting protein STAT3 Apoptosis Bax