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대장암세포주 HT-29에서 Peroxisome Proliferator-activated Receptor-γ 리간드가 Fas 매개 세포자멸사에 미치는 영향
정용우 ( Chung Yong Woo ),한동수 ( Han Dong Soo ),강은경 ( Kang Eun Kyung ),이진숙 ( Lee Jin Sook ),이항락 ( Lee Hang Rak ),김진배 ( Kim Jin Bae ),박준용 ( Park Jun Yong ),김용석 ( Kim Yong Seok ),이오영 ( Lee Oh Young ),손주현 ( 대한소화기학회 2003 대한소화기학회지 Vol.42 No.1
Background/Aims: Peroxisome proliferator-activated receptor-γ (PPAR-γ) plays a critical role in adipocytes differentiation and insulin sensitivity and is also related to regulation of inflammation and cell proliferation. The aim of this study was to investigate the PPAR-γ agonist-induced apoptosis and effects of PPAR-γ agonist on Fas-mediated apoptosis in a human colon cancer cell line. Methods: Cell survival and apoptosis of HT-29 cells were measured by trypan blue exclusion method and FACScan after treatment with 15d-PGJ2, ciglitazone and IgM anti-Fas antibody (CH11), respectively or simultaneously. Also, activation of caspase-3 and caspase-8 was analyzed to assess the effects of PPAR-γ and Fas on apoptosis signaling pathways. Results: CH11 induced apoptosis of HT-29 cells. 15d-PGJ2 or ciglitazone alone did not induce apoptosis, but combined stimulation with CH11 synergistically induced apoptosis. Also, 15d-PGJ2 alone did not activate caspase-3, but CH11 and 15d-PGJ2 synergistically activated caspase-3. CH11 activated procaspase-8, but 15d-PGJ2 did not. Conclusions: PPAR-γwas not an enough condition to induce apoptosis of HT-29 cells. Apoptosis was induced by high dose Fas, and was enhanced with PPAR-γ agonist. PPAR-γ agonist seems to enhance Fas-mediated apoptosis by affecting the way between caspase-8 and caspase-3. Further research is needed to use PPAR-γ agonists as chemopreventive and therapeutic agent for colon cancer and to find the pathways of PPAR-γ on apoptotic cascade of colon cancer cells. (Korean J Gastroenterol 2003;42:35-41)