Abstract Objective: This study aims to investigate the role of the RAD51C gene in the development of ovarian cancer. A lentivirus-based RAD51C interference system was constructed to infect A2780 cells, followed by regular screening and injection of selected cell lines into nude mice. The study also analyzed the differential expression of the RAD51C, VEGF, and NRP-2 proteins. Methods: A2780 cells were cultured, and RAD51C expression was detected. A RAD51C interference vector was constructed and packaged into a lentivirus, which was then used for cell transfection. The transfection efficiency was confirmed using qPCR, and stable cell lines were established by regular screening. A CDX model was created, and tumor formation was observed. Tumor tissues were collected and analyzed for the expression of RAD51C, VEGF, and NRP-2 proteins using Western blotting and immunohistochemistry. Results: qPCR validation demonstrated that the RAD51C lentivirus had the most significant interference effect in the SiRAN285 group. Among the CDX model groups, the Si-RAD51C group exhibited the lowest tumor volume and weight, along with significantly reduced expression of the RAD51C, NRP-2, and VEGF proteins. Conclusion: RAD51C interference lentivirus effectively inhibited the formation of A2780 ovarian cancer cell tumors and suppressed the expression of the RAD51C, NRP-2, and VEGF proteins.
No takes yet. Share an insight, caveat, or question.
Lü et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: