journal contribution
posted on 2023-03-31, 01:08 authored by Xu Yang, Gang Chen, Wei Li, Changmin Peng, Yue Zhu, Xiaoming Yang, Teng Li, Cheng Cao, Huadong Pei Supplementary data legends
Funding
National Basic Research Program of China
National Natural Science Foundation of China
Natural Science Foundation of Beijing
International S&T Cooperation Program of China
state Key Laboratory of Proteomics
History
ARTICLE ABSTRACT
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. Cancer Res; 77(5); 1142–54. ©2016 AACR.
