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Association and molecular mechanism between apoptotic regulation and chemosensitivity of esophageal cancer

Association and molecular mechanism between apoptotic regula...

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“细胞活动生命活力”——中国细胞生物学学会全体会员代表大会暨第十二次学术大会

作者： Yang Xu~1,Lanping Zhou~1,Jing Huang~1,Fang Liu~1,Jian Yu~2,Qimin Zhan~1,Lin Zhang~2,Xiaohang Zhao~1 1.State Key Laboratory of Molecular Oncology,Cancer institute & Hospital,Chinese Academy of Medical Sciences & Peking Union Medical College,Beijing 100021,China 2.University of Pittsburgh Cancer institute,and Departments of pathology and Pharmacology and Chemical Biology,University of Pittsburgh School of Medicine,Pittsburgh,pa 15213,USA

Object:To examine the expression of Smac,a proapoptotic gene,and c-iAP1,an apoptotic inhibitor protein,in the esophageal squamous cell carcinoma tissues,and investigate the molecular mechanisms of Smac and c-iAP1 regulaiton of ***:in current study,immunohistochemistry and western blot methods were used to detect the expression of Smac and c-iAP1 in tissues from ESCC and adjacent *** and gene transfection were used to select a stable clone with Smac knockdwon. Cell cytotoxity response to CDDP and long-term survival were evaluated via MTT assay, immuno-fluoresence and colony *** rate and cellular substructure detected by transmission electron microscope(TEM) and flow-cytometry with Annexin V-Pi staining,apoptosis related proteins and molecular mechanism withwestern blot *** mimetics on chemosensitivity of ESCC were *** therapeutic response of ESCC cells with different Smac status in vivo were compared using xenograft ***:We found that Smac was significantly down-regulated in esophageal cancer(64.7%,44/68,P=0.001),and Smac expression was significantly different(Pitive(with CR or PR responses) and chemoresistant(with SD or PD) *** associations of tested factors with response was tested using logistic regression *** ESCC cells treated with cisplatin,a commonly used chemotherapeutic drug,Smac and cytochrome C were released from mitochondria,in company with caspase-3 and caspase-9 *** knockdown of Smac abrogated cisplatin-induced apoptosis,mitochondrial dysfunction,cytochrome C release,and caspase *** deficiency also reduced the effect of cisplatin on long-term cell viability,and led to increase cisplatin resistance in xenograft tumors in ***,LBW242,a small molecule Smac mimetic,enhanced cisplatin-induced apoptosis and caspase activation,and restored cisplatin sensitivity in Smac-deficient ***:Our data suggested tha

关键词： Apoptosis Smac Esophageal cancer Chemosensitivity

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