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Regulation of miRNAs on c-met protein expression in ovarian cancer and its implication
1Departments of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, The Inner Mongolia Autonomous Region Tumor Hospital, The Inner Mongolia Autonomous Region Hohhot, China. qinsizxc@163.com.
Objective:
HGF/c-met signal pathway exerts important roles in tumor pathogenesis. The study of c-met related regulatory mechanism provides the basis for finding anti-tumor molecular drugs. MiRNAs can effectively regulate gene expression and work as gene therapy. The identification of miRNAs for c-met regulation and study of related mechanism are of critical importance.
Materials And Methods:
Bioinformatics approach was used to search for possible miRNAs with regulatory functions on c-met gene. Using pcDNA3.1-EGFP as the scaffold, miRNAs over-expression and inhibitor plasmids were constructed for electroporation-transfection in ovarian cell line ES-2, and pcDNA3.1-EGFP empty plasmid was used as the control group. qRT-PCR and Western blot were applied to measure c-met mRNA and protein expression, followed by transwell chamber in vitro assay for the evaluation of invasion potency.
Results:
Bioinformatics prediction showed favorable regulatory function on c-met gene by miR-204. The differential expressions of EGFP were observed between pcDNA3.1-EGFP-204-up and inhibitor plasmid pcDNA3.1-EGFP-204-down. After transfection for 24 h and 48 h, c-met expression in miR-204 over-expression group gradually decreased (p<0.05 compared to control group), accompanied with reducing cell migration or invasion potency in a time dependent manner (p<0.05). In contrast, no significant difference in the level of c-met was found in the inhibitor group and control group (p>0.05).
Conclusions:
The up-regulation of miR-204 suppressed the expression of c-met in ovarian cancer cells and inhibited cell infiltration. The suppression of miR-204 expression, however, presented no significant impact on cell infiltration potency.
Insights
MicroRNA-204 (miR-204) suppresses c-met expression and reduces ovarian cancer cell invasion. Upregulating miR-204 shows therapeutic potential, while its suppression has no significant effect on invasion.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- The HGF/c-met signaling pathway is crucial in tumor development.
- MicroRNAs (miRNAs) are key regulators of gene expression and potential therapeutic agents.
- Identifying miRNAs targeting c-met is vital for developing anti-cancer drugs.
Purpose of the Study:
- To investigate the regulatory role of miRNAs on the c-met gene.
- To explore the potential of miR-204 as a therapeutic target in ovarian cancer.
Main Methods:
- Bioinformatics analysis to predict miRNA targets of c-met.
- Construction of miR-204 overexpression and inhibitor plasmids.
- Transfection into ES-2 ovarian cancer cells.
- qRT-PCR and Western blot to assess c-met mRNA and protein levels.
- Transwell assays to evaluate cell invasion.
Main Results:
- Bioinformatics predicted miR-204 as a regulator of c-met.
- miR-204 overexpression significantly decreased c-met mRNA and protein levels in ovarian cancer cells.
- Upregulation of miR-204 reduced cell migration and invasion in a time-dependent manner.
- Inhibition of miR-204 did not significantly affect c-met levels or cell invasion.
Conclusions:
- miR-204 suppresses c-met expression and inhibits ovarian cancer cell infiltration.
- miR-204 represents a potential therapeutic strategy for ovarian cancer by targeting the HGF/c-met pathway.
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