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[MiR-125b-5 suppresses ovarian cancer cell migration and invasion by targeted downregulation of CD147]
1Department of Hematology, Hunan Provincial People's Hospital, Changsha 410005, China.
Objective:
To investigate whether miR-125b-5p regulates biological behaviors of ovarian cancer cells by targeted regulation of CD147 expression.
Methods:
RT-qPCR was used to detect the expression of miR-125b-5p and CD147 mRNA in ovarian cancer tissues and cancer cell lines. SKOV3 cells transfected with miR-125b-5p mimic and HO8910 cells transfected with miR-125b-5p inhibitor were examined for changes in proliferation, migration and invasion using CCK-8 assay, colonyforming assay and Transwell assay. Starbase was used to predict the potential binding sites between miR-125b-5p and CD147, and double luciferase reporter gene assay was used to verify the targeting relationship. In SKOV3 cells, the effects of cotransfection with miR-125b-5p mimic and pcDNA3.1-CD147 (or pcDNA3.1) plasmid on cell proliferation, migration and invasion were assessed with CCK-8 assay and Transwell assay.
Results:
The expression of miR-125b-5p was significantly lowered and that of CD147 was increased in both ovarian cancer tissues and ovarian cancer cell lines (P < 0.05). Overexpression of miR-125b-5p in SKOV3 cells resulted in significantly suppressed cell proliferation, migration and invasion, while downregulation of miR-125b-5p in HO8910 cells promoted cell proliferation, migration and invasion. Bioinformatic analysis predicted that miR-125b-5p binds to CD147, which was confirmed by luciferase reporter gene assay. RT-qPCR and Western blotting showed that miR-125b-5p negatively regulated CD147 expression (P < 0.05). In SKOV3 cells, the inhibitory effects of miR-125b-5p mimic on cell proliferation, invasion and migration were significantly attenuated by co-transfection of the cells with pcDNA3.1-CD147 plasmid.
Conclusion:
miR-125b-5p inhibits the migration and invasion of ovarian cancer cells by negatively regulating the expression of CD147.
Insights
MicroRNA-125b-5p (miR-125b-5p) inhibits ovarian cancer cell migration and invasion by downregulating CD147 expression. This finding offers a potential therapeutic target for ovarian cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Ovarian cancer is a leading cause of cancer-related death in women.
- Dysregulation of microRNAs (miRNAs) and their target genes plays a crucial role in ovarian cancer progression.
- CD147 is implicated in various cancers, but its role in ovarian cancer remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of miR-125b-5p in regulating ovarian cancer cell behaviors.
- To determine if miR-125b-5p targets CD147 expression in ovarian cancer cells.
- To explore the potential of the miR-125b-5p/CD147 axis as a therapeutic target.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) and Western blotting to assess miR-125b-5p and CD147 expression.
- Cell proliferation, migration, and invasion assays (CCK-8, colony formation, Transwell) to evaluate cellular behaviors.
- Bioinformatic prediction (Starbase) and dual-luciferase reporter assays to confirm the targeting relationship between miR-125b-5p and CD147.
- Transfection experiments with miR-125b-5p mimics/inhibitors and CD147 plasmids in ovarian cancer cell lines (SKOV3, HO8910).
Main Results:
- miR-125b-5p expression was significantly decreased, while CD147 expression was increased in ovarian cancer tissues and cell lines.
- Overexpression of miR-125b-5p suppressed ovarian cancer cell proliferation, migration, and invasion.
- Downregulation of miR-125b-5p promoted these cellular processes.
- miR-125b-5p directly targets CD147, negatively regulating its expression.
- Restoring CD147 expression attenuated the inhibitory effects of miR-125b-5p.
Conclusions:
- miR-125b-5p acts as a tumor suppressor in ovarian cancer.
- The miR-125b-5p/CD147 axis is a critical regulator of ovarian cancer cell migration and invasion.
- Targeting this pathway holds promise for novel ovarian cancer therapies.
