miR-200b regulates breast cancer cell proliferation and invasion by targeting radixin

• Published in: Experimental and therapeutic medicine Vol. 19; no. 4; pp. 2741 - 2750
• Main Authors: Yuan, Jianfen, Xiao, Chunhong, Lu, Huijun, Yu, HaizHong, Hong, Hong, Guo, Chunyan, Wu, Zhimei
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.04.2020; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Apoptosis; Breast cancer; Cancer cells; Cancer metastasis; Cell culture; Cell growth; Chinese medicine; Computational biology; Gene expression; Genetic engineering; Hyperplasia; Immunoglobulins; Messenger RNA; Metastasis; MicroRNA; MicroRNAs; Pathogenesis; Photographic industry; Plasmids; Polymerase chain reaction; Proteins; RNA; Scientific equipment industry; Signal transduction; Studies; Tumors; Womens health; Canada; United States; Japan; Beijing China; China; breast cancer; invasion; proliferation; radixin; microRNA-200b
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2020.8516

Radixin is an important member of the Ezrin-Radixin-Moesin protein family that is involved in cell invasion, metastasis and movement. microRNA (miR)-200b is a well-studied microRNA associated with the development of multiple tumors. Previous bioinformatics analysis has demonstrated that miR-200b has a complementary binding site in the 3'-untranslated region of radixin mRNA. The present study aimed to investigate the role of miR-200b in regulating radixin expression, cell proliferation and invasion in breast cancer. Breast cancer tissues at different Tumor-Node-Metastasis (TNM) stages were collected; breast tissues from patients with hyperplasia were used as a control. miR-200b and radixin mRNA expression levels were tested by reverse transcription-quantitative PCR. Radixin protein expression was detected by western blotting. The highly metastatic MDA-MB-231 cells were divided into four groups and transfected with a miR-negative control (NC), miR-200b mimic, small interfering (si)RNA-NC or siRNA targeting radixin. Cell invasion was evaluated by Transwell assay and cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine staining. Compared with the control group, radixin mRNA expression was significantly higher in breast cancer tissues and increased with TNM stage. miR-200b expression levels exhibited the opposite trend. Radixin mRNA expression in breast cancer cells was notably higher, whereas miR-200b expression was lower compared with that in normal breast epithelial MCF-10A cells. The expression of radixin was higher, whereas miR-200b was lower in MDA-MB-231 cells compared with that in MCF-7 cells. miR-200b mimic or siRNA-radixin transfection downregulated the expression of radixin in MDA-MB-231 cells and attenuated the invasive and proliferative abilities of these cells. miR-200b-knockdown and radixin overexpression were associated with enhanced cell invasion in breast cancer. In conclusion, miR-200b regulates breast cancer cell proliferation and invasion by targeting radixin expression.