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Overexpression of mir-183 and mir-494 promotes proliferation and migration in human breast cancer cell lines
- Source :
- Oncology Letters. 14:1054-1060
- Publication Year :
- 2017
- Publisher :
- Spandidos Publications, 2017.
-
Abstract
- Breast cancer (BC) is a leading cause of cancer-associated mortality in females worldwide. MicroRNAs (miRNAs or miRs), a type of non-coding RNA, have been reported to be important in the regulation of BC onset and progression. Several studies have implicated the role of miR-183 and miR-494 in different types of cancer. However, the biological functions of these miRNAs in BC remain largely unknown. In the present study, the expression of both miRNAs was assessed in the MDA-MB-231 and MDA-MB-468 BC cell lines. It was hypothesized that miR-183 and miR-494 serve an important role in regulating the expression of key genes associated with the metastatic phenotype of BC cells. To further understand their role, the expression of these miRNAs was restored in selected BC cell lines. Functional assays revealed that overexpression of miR-183 or miR-494 modulated the proliferation and migration of MDA-MB-231 and MDA-MB-468 cells in vitro. Additionally, retinoblastoma 1 (RB1) was identified to be a downstream target of both miRNAs by in silico analysis. Western blotting revealed that upregulation of miR-183 was associated with downregulation of RB1 protein in MDA-MB-231 cells. In conclusion, the present results support the hypothesis that miR-183 and miR-494 serve a pivotal role in BC metastasis, and that miR-183 may act as an oncogene by targeting RB1 protein in MDA-MB-231 cells.
- Subjects :
- 0301 basic medicine
Cancer Research
Oncogene
Cell
Cancer
Articles
Biology
Cell cycle
medicine.disease
medicine.disease_cause
Metastasis
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
medicine.anatomical_structure
Oncology
Downregulation and upregulation
030220 oncology & carcinogenesis
microRNA
Cancer research
medicine
Carcinogenesis
Subjects
Details
- ISSN :
- 17921082 and 17921074
- Volume :
- 14
- Database :
- OpenAIRE
- Journal :
- Oncology Letters
- Accession number :
- edsair.doi.dedup.....7e054ed7a1320bb9841318f096e3afeb