期刊
CANCER RESEARCH
卷 77, 期 5, 页码 1142-1154出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-16-1378
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资金
- National Basic Research Program of China [2015CB910600, 2013CB910300]
- National Natural Science Foundation of China [31371433, 31671414, 81572740, 81602796]
- Natural Science Foundation of Beijing [5152009]
- International S&T Cooperation Program of China [2015DFA31680, 2015DFA30610]
- state Key Laboratory of Proteomics [SKLP-O201303]
- One Thousand Young Talent Program
The nonreceptor tyrosine kinase c-ABL controls cell growth but its contributions in solid tumors are not fully understood. Here we report that the Polo-like kinase PLK1, an essential mitotic kinase regulator, is an important downstream effector of c-ABL in regulating the growth of cervical cancer. c-ABL interacted with and phosphorylated PLK1. Phosphorylation of PLK1 by c-ABL inhibited PLK1 ubiquitination and degradation and enhanced its activity, leading to cell-cycle progression and tumor growth. Both c-ABL and PLK1 were overexpressed in cervical carcinoma. Notably, PLK1 tyrosine phosphorylation correlated with patient survival in cervical cancer. In a murine xenograft model of human cervical cancer, combination treatment with c-ABL and PLK1 inhibitors yielded additive effects on tumor growth inhibition. Our findings highlight the c-ABL-PLK1 axis as a novel prognostic marker and treatment target for human cervical cancers. (C) 2016 AACR.
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