Study on the Mechanism of Cell Cycle Checkpoint Kinase 2 (CHEK2) Gene Dysfunction in Chemotherapeutic Drug Resistance of Triple Negative Breast Cancer Cells

• DOI: 10.12659/msm.907256
• Publication Date: 2018-05-15T07:14:16Z
• Authors: Li Luo; Wei Gao; Jinghui Wang; Dingxue Wang; Xiaobo Peng; Zhaoyang Jia; Ye Jiang; Gongzhuo Li; Dongxin Tang; Yajie Wang
• Keywords: CHEK2; Viability assay; Checkpoint Kinase 2; MTT assay

BACKGROUND This study aimed to investigate the mechanism of CHEK2 gene dysfunction in drug resistance triple negative breast cancer (TNBC) cells. MATERIAL AND METHODS To perform our study, a stable wild type (CHEK2 WT) or Y390C mutation Y390C) expressed MDA-MB-231 cell line was established. MTT assay, apoptosis assay and cycle were carried out analyze viability, apoptosis, respectively. Western blotting qRT-PCR applied for related protein expression detection. RESULTS We found that IC50 value DDP (Cisplatin) cells significantly higher than WT control After treatment with 48 h, expressing showed lower viability cells; compared cells, significant G1/S arrest. Meanwhile, we increased Moreover, results suggested level p-CDC25A, p-p53, p21, Bax, PUMA, Noxa CONCLUSIONS Our findings indicated induced TNBC chemotherapeutic drugs through administrating arrest via regulating p53 activation CHEK2-p53 pathway.