Knockdown of RFC2 Prevents the Proliferation, Migration and Invasion of Cervical Cancer Cells

Background/Aim: Replication factor C subunit 2 (RFC2) is a component of the replication factor C (RFC) complex, which plays a critical role in DNA replication and repair. Recent studies have reported the involvement of RFC2 in several cancers. In this study, we investigated the functional role of RFC2 in cervical cancer progression.

Materials and Methods: RFC2 expression in cervical cancer cells was analyzed using quantitative real-time PCR (qRT-PCR) and western blotting. HeLa, ME-180, and SiHa cells were transfected with siRNAs targeting RFC2. Cell viability and proliferation were assessed using the MTT and colony formation assays, and cell cycle distribution was analyzed by flow cytometry. Migration and invasion abilities were evaluated through Transwell assays with or without Matrigel.

Results: RFC2 knockdown significantly reduced cell proliferation in cervical cancer cells. Flow cytometry analysis revealed cell cycle arrest at the S phase. Additionally, RFC2 knockdown markedly inhibited the migration and invasion of cervical cancer cells. These results demonstrate the critical involvement of RFC2 in regulating proliferation and metastatic potential in cervical cancer cells.

Conclusion: RFC2 plays a pivotal role in promoting cervical cancer progression by enhancing cell growth, regulating the cell cycle, and promoting metastatic behavior. Further studies on the molecular mechanisms of RFC2 in cancer-associated pathways may provide a novel therapeutic target for developing cervical cancer treatment strategies.