Overexpression of cyclin B1 antagonizes chemotherapeutic-induced apoptosis through PTEN/Akt pathway in human esophageal squamous cell carcinoma cells

Yunwei Ou(Capital University), Liying Ma(Capital Medical University), Ling Ma(Capital University), Zhen Huang(Chinese Academy of Medical Sciences & Peking Union Medical College), Wei Zhou(Chinese Academy of Medical Sciences & Peking Union Medical College), Chunling Zhao(Chinese Academy of Medical Sciences & Peking Union Medical College), Bailin Zhang(Chinese Academy of Medical Sciences & Peking Union Medical College), Yongmei Song(Chinese Academy of Medical Sciences & Peking Union Medical College), Chunjiang Yu(Capital University), Qimin Zhan(Chinese Academy of Medical Sciences & Peking Union Medical College)
Cancer Biology & Therapy
January 1, 2013
Cited by 38Open Access
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Abstract

The role of cyclin B1 in the clinical therapeutic sensitivity of human esophageal squamous cell carcinoma (ESCC) remains to be defined. In this study, we found that elevated cyclin B1 expression attenuated the apoptosis induced by cisplatin or paclitaxel, while knockdown of cyclin B1 enhanced cisplatin or paclitaxel sensitivity in ESCC cells. Cyclin B1-mediated apoptosis may rely on the Bcl-2-dependent mitochondria-regulated intrinsic death pathway, and the antagonizing effect of cyclin B1 on chemotherapeutic agent-induced apoptosis was through PTEN/Akt pathway. Therefore, cyclin B1 might be a therapeutic target for the development of specific and efficient approaches in the treatment of ESCC.


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