Abstract:
:MicroRNA-342-3p (miR-342) has been shown to act as a tumor-suppressor in different cancer types. However, the role and therapeutic implications of miR-342 via modulation of Cofilin 1 (CFL1) has not been studied in any type of cancer. Given the importance of Cofilin signalling in breast, this study was undertaken to explore the therapeutic implications of miR-342 and its target CFL1 in breast cancer. Herein, we found that miR-342 was significantly (P < 0.05) downregulated in breast cancer tissues and cell lines. Functional assays revealed that overexpression of miR-342 caused a significant (P < 0.05) inhibition of the proliferation, colony formation, invasion and migration of the MDA-MB-436 and CAMA-1 breast cancer cells via induction of apoptosis. Bioinformatic approaches and the dual luciferase reporter assay confirmed the interaction between miR-342 and its target CFL1. Moreover, we found that CFL1 was aberrantly overexpressed in breast cancer tissues and cell lines. Overexpression of miR-342 caused remarkable depletion in the expression of CFL1 in MDA-MB-436 breast cancer cells. Silencing of CFL1 in CAMA-1 and MDA-MB-436 cells caused remarkable decrease in the proliferation, colony formation and migration of these cells, similar to that of miR-342 ovexpression. However, overexpression of CFL1 in MDA-MB-346 cells could avoid the tumor suppressive effects of miR-342. Our data provide novel information about the implications of miR-342 and its target CFL1 in breast cancer treatment.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Liu C,Xing H,Luo X,Wang Ydoi
10.1016/j.abb.2020.108385subject
Has Abstractpub_date
2020-07-15 00:00:00pages
108385eissn
0003-9861issn
1096-0384pii
S0003-9861(20)30394-5journal_volume
687pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2008-08-15 00:00:00