BCL‐XL binds and antagonizes RASSF6 tumor suppressor to suppress p53 expression |
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| Authors: | Xiaoyin Xu Hiroaki Iwasa Shakhawoat Hossain Aradhan Sarkar Junichi Maruyama Kyoko Arimoto‐Matsuzaki Yutaka Hata |
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| Affiliation: | 1. Department of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan;2. Department of Breast Oncology Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China;3. Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh;4. Center for Brain Integration Research, Tokyo Medical and Dental University, Tokyo, Japan |
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| Abstract: | RASSF6, a member of the tumor suppressor Ras‐association domain family proteins, induces apoptosis in the caspase‐dependent and caspase‐independent manners. RASSF6 interacts with MDM2 and stabilizes p53. BCL‐XL is a prosurvival member of BCL‐2 family proteins. BCL‐XL directly inhibits proapoptotic BAX and BAK. BCL‐XL also traps tBID, a proapoptotic activator BH3‐only protein, and sequesters p53. In addition, BCL‐XL regulates the mitochondrial membrane permeability via voltage‐dependent anion channel. In these manners, BCL‐XL plays an antiapoptotic role. We report the interaction of BCL‐XL with RASSF6. BCL‐XL inhibits the interaction between RASSF6 and MDM2 and suppresses p53 expression. Consequently, BCL‐XL antagonizes RASSF6‐mediated apoptosis. Thus, the inhibition of RASSF6‐mediated apoptosis also underlies the prosurvival role of BCL‐XL. |
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| Keywords: | apoptosis BCL‐XL p53 |
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