Abstract |
The present study aimed to investigate the functional effects of microRNA‑195 on ovarian cancer cells and the underling mechanism involved. Reverse transcription‑quantitative polymerase chain reaction was used to measure the expression of microRNA‑195 in patients with ovarian cancer. Cell proliferation and apoptosis were measured with MTT assay and flow cytometry, respectively. Caspase‑3/9 activity, vascular endothelial growth factor receptor (VEGFR)2 and phosphorylated protein kinase B (p‑AKT) protein expression were analyzed using caspase‑3/9 activity kits and western blot analysis. The expression of microRNA‑195 was downregulated in ovarian cancer, compared with the normal control group. Furthermore, microRNA‑195 suppresses cell proliferation and induced apoptosis of ovarian cancer cells. In addition, microRNA‑195 suppressed VEGFR2 and p‑AKT protein expression in ovarian cancer cells. The inhibition of VEGFR2 and p‑AKT increased the functional effects of microRNA‑195 on apoptosis of ovarian cancer cells. The results demonstrated that microRNA‑195 suppresses cell proliferation of ovarian cancer cells through regulation of VEGFR2 and AKT signaling pathways.
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Authors | Jun Chen |
Journal | Molecular medicine reports
(Mol Med Rep)
Vol. 18
Issue 2
Pg. 1666-1673
(Aug 2018)
ISSN: 1791-3004 [Electronic] Greece |
PMID | 29845300
(Publication Type: Journal Article)
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Chemical References |
- MIRN195 microRNA, human
- MicroRNAs
- KDR protein, human
- Vascular Endothelial Growth Factor Receptor-2
- Proto-Oncogene Proteins c-akt
- CASP3 protein, human
- CASP9 protein, human
- Caspase 3
- Caspase 9
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Topics |
- Adenocarcinoma
(genetics, metabolism, pathology)
- Adult
- Apoptosis
- Carcinoma
(genetics, metabolism, pathology)
- Case-Control Studies
- Caspase 3
(genetics, metabolism)
- Caspase 9
(genetics, metabolism)
- Cell Line, Tumor
- Cell Proliferation
- Female
- Gene Expression Regulation, Neoplastic
- Humans
- MicroRNAs
(genetics, metabolism)
- Middle Aged
- Neoplasm Staging
- Ovarian Neoplasms
(genetics, metabolism, pathology)
- Proto-Oncogene Proteins c-akt
(genetics, metabolism)
- Signal Transduction
- Vascular Endothelial Growth Factor Receptor-2
(genetics, metabolism)
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