Title |
MicroRNA-214-3p inhibits proliferation and cell cycle progression by targeting MELK in hepatocellular carcinoma and correlates cancer prognosis
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Published in |
Cancer Cell International, November 2017
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DOI | 10.1186/s12935-017-0471-1 |
Pubmed ID | |
Authors |
Yue Li, You Li, Yao Chen, Qian Xie, Ningning Dong, Yanjun Gao, Huan Deng, Chunhua Lu, Suihai Wang |
Abstract |
MicroRNAs are considered as potential regulators in various biological pathways and contribute to the diagnosis and prognosis of cancers. MicroRNA-214-3p (miR-214-3p) was proved to be correlated with various cancers in recent studies. However, the biological functions of miR-214-3p in hepatocellular carcinoma (HCC) and its association with the prognosis of HCC after liver transplantation are still unevaluated. Here we intended to elucidate the functional implication of miR-214-3p in regulation of cell proliferation and apoptosis and its potential prediction of clinical prognosis of HCC patients. Expressions of miR-214-3p in 98 HCC patients and three HCC cell lines were detected by quantitative reverse transcription PCR (qRT-PCR) to explore the association of miR-214-3p expression and clinicopathological characteristics. The effects of miR-214-3p on cell proliferation and apoptosis were examined by proliferation and flow cytometry assay, respectively. The direct target gene of miR-214-3p was also detected by luciferase reporter assay. The effects of miR-214-3p on cell proliferation and apoptosis were examined by proliferation and flow cytometry assay, respectively. The direct target gene of miR-214-3p was also detected by luciferase reporter assay. The results showed that miR-214-3p expression was downregulated in primary HCC samples compared with normal liver tissues, and was decreased in HCC recurrence species compared with non-recurrence controls (P = 0.001). Low miR-214-3p level was associated with poor overall survival (OS) (Log rank P = 0.003) and recurrence-free survival (RFS) (Log rank P = 0.007). Moreover, miR-214-3p precursor transfection resulted in decreased cell proliferation, cell cycle arrest at G1 phase, and enhanced cell apoptosis in HepG2 and HUH-7 cells. Further investigation showed that miR-214-3p could regulate its target gene maternal embryonic leucine zipper kinase (MELK) by directly binding to MELK-3'-UTR. miR-214-3p suppresses HCC progression by directly down-regulating MELK expression, indicating a potential therapeutic target for the treatment and prognosis of HCC patients. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 16 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 5 | 31% |
Other | 2 | 13% |
Researcher | 2 | 13% |
Professor | 1 | 6% |
Student > Doctoral Student | 1 | 6% |
Other | 2 | 13% |
Unknown | 3 | 19% |
Readers by discipline | Count | As % |
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Biochemistry, Genetics and Molecular Biology | 6 | 38% |
Agricultural and Biological Sciences | 1 | 6% |
Immunology and Microbiology | 1 | 6% |
Unknown | 8 | 50% |