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Published on: August 2, 2024
MicroRNA-331-3p inhibits proliferation and metastasis of ovarian cancer by targeting RCC2
Gulimire Buranjiang1, Reziya Kuerban2, Ailikemu Abuduwanke3
1Department of Gynecologic Oncology Radiation Therapy (Ward II), Xinjiang Medical University Third Clinical Medical College (Affiliated Tumor Hospital), Urumqi, Xinjiang, China.
Introduction:
Epithelial ovarian carcinoma (EOC) is one of the most lethal gynecologic malignancies, with a poor 5-year survival rate. Numerous studies have shown that microRNAs participate in the malignant behavior of ovarian cancer cells by directly targeting multiple oncogenes or tumor suppressor genes.
Material And Methods:
Reverse transcription-PCR was used to determine the level of miR-331-3p in EOC. Cells proliferation was measured with the Cell Counting Kit-8. Cell mobility were measured by wound-healing assay. Cell migration and invasion were measured by transwell assay. Luciferase assays were used to demonstrate that RCC2 was a directed target of miR-331-3p in EOC. Western blots were used to measure the protein expression.
Results:
We found that the expression of microRNA-331-3p (miR-331-3p) in ovarian cancer cell lines is reduced (p < 0.01), and an increase of expression of miR-331-3p in ovarian cancer cells significantly inhibits cell proliferation (p < 0.001). Transwell and wound-healing assays showed that miR-331-3p inhibits the cell motility of ovarian cancer cells (p < 0.001). Regulator of chromosome condensation 2 (RCC2) was predicted to be a novel target for miR-331-3p. Our luciferase activity assay confirmed that RCC2 is directly targeted by miR-331-3p. RCC2 was negatively regulated by miR-331-3p (p < 0.001), and overexpression of RCC2 could restore the malignant behaviors of ovarian cancer cells, which was suppressed by miR-331-3p.
Conclusions:
These data indicate that miR-331-3p can inhibit proliferation, migration, and invasion of ovarian cancer cells via directly targeting RCC2. Our study provides potential therapeutic targets for the treatment of ovarian cancer.
Insights
MicroRNA-331-3p (miR-331-3p) is downregulated in ovarian cancer. Restoring miR-331-3p inhibits cancer cell proliferation, migration, and invasion by targeting RCC2, offering potential therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Epithelial ovarian carcinoma (EOC) is a highly lethal gynecologic malignancy with poor survival rates.
- MicroRNAs play critical roles in ovarian cancer progression by regulating oncogenes and tumor suppressor genes.
Purpose of the Study:
- To investigate the role of microRNA-331-3p (miR-331-3p) in epithelial ovarian carcinoma.
- To identify the molecular targets of miR-331-3p in ovarian cancer cells.
Main Methods:
- Quantitative reverse transcription-PCR to assess miR-331-3p expression levels.
- Cell Counting Kit-8, wound-healing, and transwell assays to evaluate cell proliferation, motility, migration, and invasion.
- Luciferase assays and Western blotting to confirm direct targeting of RCC2 by miR-331-3p and assess protein expression.
Main Results:
- miR-331-3p expression is significantly reduced in ovarian cancer cell lines.
- Overexpression of miR-331-3p suppressed ovarian cancer cell proliferation, migration, and invasion.
- Regulator of chromosome condensation 2 (RCC2) was identified as a direct target of miR-331-3p, and its expression was negatively regulated by miR-331-3p.
Conclusions:
- miR-331-3p inhibits ovarian cancer cell proliferation, migration, and invasion by directly targeting RCC2.
- miR-331-3p and its regulatory pathway represent potential therapeutic targets for ovarian cancer treatment.
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