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Sulindac¿¡ ÀÇÇÑ ´ëÀå¾Ï ¼¼Æ÷ÁÖ HT-29 ¼¼Æ÷ÀÇ ¼¼Æ÷»ç¸ê ±âÀÛ ¿¬±¸-¹ÌÅäÄܵ帮¾Æ Åë·Î¸¦ Áß½ÉÀ¸·Î Sulindac-induced Apoptosis without Oligonucleosomal DNA Fragmentation in HT-29 Cells-Its Special References to Mitochondrial Pathway -

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±ÇÀ° ( Kwon Yuk ) 
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±è¼ºÈç ( Kim Sung-Heun ) 
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±è¹ÎÂù ( Kim Min-Chan ) 
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ÃÖÈ«Á¶ ( Choi Hong-Jo ) 
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±è¿µÈÆ ( Kim Young-Hoon ) 
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Á¶¼¼Çå ( Joh Se-Heon ) 
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Á¤°©Áß ( Jung Ghap-Joong ) 
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±è¼ºÇö ( Kim Sung-Hyun ) 
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Abstract


Purpose: This study was undertaken to reveal the molecular mechanism underlying sulindac-induced apoptosis in the human colon cancer cell line HT-29 (mutant p53).

Methods: Apoptosis was determined by using Hoechst 33342 staining, and translocation of proteins was established by using immunofluorescence, immunoelectron microscopy, and Western blotting after ultra- fractionation.

Results: This type of apoptosis was associated with decreased mitochondrial membrane potential, a translocation of the apoptosis-inducing factor (AIF) to the nucleus, and morphological evidence of nuclear condensation. However, DNA electrophoresis did not elucidate the ladder pattern of DNA fragments. Instead, a pulse-field gel electrophoresis showed that sulindac led to disintegration of nuclear DNA into-high- molecular-weight DNA fragments of about 100¢¦300 kbp.

Conclusions: Our findings indicate that sulindac induces large-scale DNA fragmentation, suggesting a predominantly AIF-mediated cell-death process, through translocation of the AIF to the nucleus in HT-29 cells. J Korean Soc Coloproctol 2004;20:191-198

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¼¼Æ÷»ç¸ê;´ëÀå¾Ï¼¼Æ÷ÁÖ HT-29; ¼¼Æ÷»ç¸ê À¯¹ßÀÎÀÚ;°íºÐÀÚ DNAÁ¶°¢
Apoptosis;Colon cancer cell line HT-29;AIF;HMW DNA fragmentation

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