Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast cancer.
Eur Rev Med Pharmacol Sci
; 22(23): 8383-8390, 2018 12.
Article
in En
| MEDLINE
| ID: mdl-30556879
OBJECTIVE: Breast cancer is one of the most common malignancies worldwide. MicroRNAs (MiRNAs) have been identified to influence cell behaviors through epigenetic post-transcriptional gene regulation. Therefore, the aim of this study was to determine the role of miR-3196 in the proliferation and apoptosis of breast cancer. MATERIALS AND METHODS: Human breast cancer cell lines (MCF-7 and MDA-MB-231) were obtained and cultured. The expression level of miR-3196 in breast cancer tissues was detected using Real Time-Polymerase Chain Reaction (RT-PCR). The effects of miR-3196 on the proliferation and apoptosis of breast cancer cells were analyzed by cell counting kit-8 (CCK-8) assay and TUNEL assay, respectively. In addition, the interaction between miR-3196 expression and erb-b2 receptor tyrosine kinase 3 (ERBB3) expression, as well as the mechanism of miR-3196 regulating ERBB3 in breast cancer, were also addressed by RT-PCR, Western blot, and luciferase reporter gene assay. RESULTS: MiR-3196 was lowly expressed in breast cancer tissues. Overexpression of miR-3196 could repress the proliferation and induce the apoptosis of breast cancer cells via targeting the 3'UTR of ERBB3. CONCLUSIONS: Our findings provide novel insights into the role of miR-3196 in breast cell proliferation and apoptosis. Meanwhile, this study suggests that miR-3196 can serve as a potential biomarker and therapeutic target for breast cancer.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Breast Neoplasms
/
Apoptosis
/
Receptor, ErbB-3
/
MicroRNAs
/
Cell Proliferation
Type of study:
Prognostic_studies
Limits:
Female
/
Humans
Language:
En
Journal:
Eur Rev Med Pharmacol Sci
Journal subject:
FARMACOLOGIA
/
TOXICOLOGIA
Year:
2018
Document type:
Article
Affiliation country:
China
Country of publication:
Italy