Molecular mechanism of miR‐153 inhibiting migration, invasion and epithelial‐mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF‐β) signaling pathway. Issue 6 (7th December 2018)

• Record Type: Journal Article
• Authors: Wang, Jingwei; Liang, Shuhang; Duan, Xiuqing
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 6(2019)
• Page Start: 9539
• Page End: 9546
• Publication Date: 2018-12-07
• Subjects: epithelial‐mesenchymal transition (EMT) -- invasion -- migration -- miR‐153 -- transforming growth factor beta receptor 2 (TGFBR2); Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.28230
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Objective: To investigate the role and mechanism of action of miR‐153 in the migration, invasion, and epithelial‐mesenchymal transition (EMT) of breast cancer cells. Methods: Quantitative real time polymerase chain reaction (qRT‐PCR) was used to detect the expression of miR‐153 and transforming growth factor beta receptor 2 (TGFBR2) in tissue specimens and cells. miR‐153 overexpression in breast cancer cells was achieved by miR‐153 mimic transfection. Mobility and invasiveness of breast cancer cells were evaluated by transwell assay. EMT was evaluated by Western blot detecting the protein level of E‐cadherin and Vimentin. Interaction of miR‐153 and 3′‐untranslated region (UTR) of TGFBR2 messenger RNA (mRNA) was investigated by luciferase reporter assay. Results: The expression of miR‐153 in breast cancer tissue specimens and MDA‐MB‐231 cells was significantly lower than that in nonmalignant counterparts, inversely correlating with that of TGFBR2 mRNA. Transfection with miR‐153 mimic significantly increased miR‐153 level in MDA‐MB‐231 cells while inhibiting its migration, invasion, and EMT in vitro, which could be mimicked by TGFBR2 knockdown. Luciferase reporter assay confirmed two targets of miR‐153 on the 3′‐UTR of TGFBR2 mRNA. Restoring TGFBR2 protein level by transient overexpression largely rescued migration, invasion, and EMT of MDA‐MB‐231 cells that were repressed by miR‐153 mimic transfection. Conclusion: miR‐153 inhibits breast cancer cell migration, invasion, and EMT by targeting TGFBR2. Abstract : miR‐153 inhibits breast cancer cell migration, invasion and epithelial‐mesenchymal transition (EMT) by targeting TGF‐β signaling pathway, and transforming growth factor beta receptor 2 (TGFBR2) is a direct target of miR‐153 in TGF‐β signaling pathway