Gain-of-function mutant p53-R280K mediates survival of breast cancer cells |
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Authors: | Yun-Hee Bae Jong-Myung Shin Hyun-Joo Park Hye-Ock Jang Moon-Kyoung Bae Soo-Kyung Bae |
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Institution: | 1. Department of Dental Pharmacology, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Yangsan, 626-870, South Korea 2. Department of Oral Physiology, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Yangsan, 626-870, South Korea
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Abstract: | Missense mutations in TP53 resulting in the expression of p53-R175H, p53-R273H, or p53-R280K are frequently detected in human breast cancer. Currently, the role of mutant p53-R280K in breast cancer is relatively unknown, and therefore, the present study analyzed the function of mutant p53-R280K in breast cancer cell growth. To this end, we used small interfering RNA to study the role of mutant p53-R280K in MDA-MB-231 cells, which endogenously express the mutant protein. We found that curcumin induced apoptosis in MDA-MB-231 cells and downregulated mutant p53-R280K. We also observed that knockdown of mutant p53 by small interfering RNA induced apoptosis in MDA-MB-231 cells. Curcumin-induced apoptosis was further enhanced by the overexpression of wild-type p53, but was decreased by mutant p53-R280K overexpression. Our findings indicate that mutant p53-R280K has an important role in mediating the survival of triple-negative breast cancer MDA-MB-231 cells. Furthermore, this study suggests mutant p53-R280K could be used as a therapeutic target for breast cancer cells harboring this TP53 missense mutation. |
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