난소암 세포에서 IEX-1과 MCL-1 단백질들의 세포사멸 기능에 관한 상호작용
Mutual Activities of IEX-1 and MCL-1 on the Apoptosis of Ovarian Cancer Cells
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Apoptosis is a crucial mechanism for the proper regulation of homeostasis. BCL-2 family proteins are key molecules which control cellular survival and apoptosis. MCL-1(myeloid cell leukemia-1) is a pro-survival member of BCL- 2 family that promotes the survival of cells, and is highly expressed in diverse cancers including ovarian cancer, leukemia, and cervical cancer. Previously we identified IEX-1(immediate early response gene X-1) as a binding partner of MCL- 1. In the present study, we demonstrated that overexpression of IEX-1 induces apoptosis of ovarian cancer cells. Moreover, IEX-1 significantly attenuated the pro-survival function of MCL-1 in these cells. Also, IEX-1-induced cell death activity was able to be modulated by changes in the expression level of MCL-1. Thus, these results suggest that both IEX-1 and MCL-1 modulate each other’s function controlling cellular survival and death and the inhibitory activity of IEX-1 toward MCL-1 may be applied for the development of chemotherapeutics.
Abstract
Apoptosis is a crucial mechanism for the proper regulation of homeostasis. BCL-2 family proteins are key molecules which control cellular survival and apoptosis. MCL-1(myeloid cell leukemia-1) is a pro-survival member of BCL- 2 family that promotes the survival of cells, and is highly expressed in diverse cancers including ovarian cancer, leukemia, and cervical cancer. Previously we identified IEX-1(immediate early response gene X-1) as a binding partner of MCL- 1. In the present study, we demonstrated that overexpression of IEX-1 induces apoptosis of ovarian cancer cells. Moreover, IEX-1 significantly attenuated the pro-survival function of MCL-1 in these cells. Also, IEX-1-induced cell death activity was able to be modulated by changes in the expression level of MCL-1. Thus, these results suggest that both IEX-1 and MCL-1 modulate each other’s function controlling cellular survival and death and the inhibitory activity of IEX-1 toward MCL-1 may be applied for the development of chemotherapeutics.
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