LncRNA BCAR4 promotes migration, invasion, and chemo-resistance by inhibiting miR-644a in breast cancer.

Autor: Wu, Tangwei, Li, Xiaoyi, Yan, Ge, Tan, Zheqiong, Zhao, Dan, Liu, Shuiyi, Wang, Hui, Xiang, Yuan, Chen, Weiqun, Lu, Hongda, Liao, Xinghua, Li, Yong, Lu, Zhongxin
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Zdroj: Journal of Experimental & Clinical Cancer Research (17569966); 1/10/2023, Vol. 42 Issue 1, p1-15, 15p
Abstrakt: Background: Metastasis and drug resistance of breast cancer have become a barrier to treating patients successfully. Long noncoding RNAs (lncRNAs) are known as vital players in cancer development and progression. Methods: The RT-qPCR were used to detect the gene expression. Colony formation assay, would healing assay, and transwell assay were performed to investigate oncogenic functions of cells. CCK8 assay was used to detect the cell viability. Western blot was applied to detect the protein level. Dual-luciferase reporter assay was used to determine the relationship between molecules. Mouse orthotopic xenograft tumor models were established to evaluate the effects of BCAR4 on tumor growth and metastasis in vivo. Results: LncRNA BCAR4 was significantly increased in breast cancer patients' tissues and plasma and upregulated in breast cancer cell lines. BCAR4 upregulation was correlated with the TNM stages and decreased after surgical removal of breast tumors. Silencing of BCAR4 suppressed breast cancer cell colony formation, migration, invasion, and xenograft tumor growth and promoted chemo-sensitivity. Mechanistically, BCAR4 facilitates breast cancer migration and invasion via the miR-644a-CCR7 axis of the MAPK pathway. BCAR4 promotes ABCB1 expression indirectly by binding to and down-regulating miR-644a to induce chemo-resistance in breast cancer. Conclusions: Our findings provide insights into the oncogenic role of BCAR4 and implicate BCAR4 as a potential diagnostic biomarker and a promising therapeutic agent to suppress metastasis and inhibit chemo-resistance of breast cancer. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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