Role and Regulatory Mechanism of LGR5 in the Occurrence and Development of Breast Cancer
Role and Regulatory Mechanism of LGR5 in the Occurrence and Development of Breast Cancer
Yajuan Zheng, Qiuping Mo, Hongchao Tang, Qinghui Zheng and Dandan Guan*
ABSTRACT
Breast cancer is a phenomenon in which mammary epithelial cells proliferate out of control under the action of various carcinogenic factors. This study aimed to explore the role and regulatory mechanism of LGR5 in the occurrence and development of breast cancer. Fresh breast cancer case samples and normal breast cell samples were collected. Western blot was used to analyze the expression of LGR5 and (phosphorylated IQGAP1)/(IQGAP1). Construct metastatic human breast cancer MDA-MB-231 cell line knocking down LGR5. The relative expression levels of LGR5 and phosphorylated IQGAP1 were detected by Western blot. The relative activity of the above three types of cells after 24 h of culture was detected by CCK8 assay. The migration ability of the cells was analyzed by the cell scratch test, and the invasive ability of the cells was analyzed by the transwell detection. Construct LGR5-knockdown, LGR5-overexpressing and LGR5-ΔC-overexpressing (lack of C-terminal tail) human colon cancer LoVo cell lines. The mechanism of the reaction between LGR5 and IQGAP1 was examined by immunoprecipitation. Expression of LGR5 and phosphorylation ratio of IQGAP1 showed opposite trends in breast cancer and normal body. Viability, migration and invasion ability of breast cancer cells were all affected by LGR5 expression and IQGAP1 phosphorylation ratio. LGR5 affected IQGAP1 phosphorylation process by linking to IQGAP1 through its own C-terminus. This study proved that LGR5, which is highly expressed in breast cancer cells, interacts with IQGAP1 through its C-terminal end, reducing the phosphorylation ratio of IQGAP1, thereby improving the viability, migration and invasion ability of breast cancer cells, and ultimately increasing the malignant transformation rate of breast cancer.
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