التفاصيل البيبلوغرافية
| العنوان: |
MicroRNA-342 targets Cofilin 1 to suppress the growth, migration and invasion of human breast cancer cells. |
| المؤلفون: |
Liu, Cong1 (AUTHOR), Xing, Hua1 (AUTHOR), Luo, Xiao1 (AUTHOR), Wang, Yimin1,2 (AUTHOR) yiminwang@jlu.edu.cn |
| المصدر: |
Archives of Biochemistry & Biophysics. Jul2020, Vol. 687, pN.PAG-N.PAG. 1p. |
| مصطلحات موضوعية: |
*BREAST cancer, *CANCER cells, *CELL migration inhibition, *CANCER cell migration, *CELL migration, *CELL lines |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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