ArticleCancer genomics & proteomics
Replication Factor C Subunit 4 Plays a Role in Human Breast Cancer Cell Progression.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- First genome report ofFrontiers in fungal biology · 2026Article
- Multiple roles of replication factor C family in pan‑cancer (Review).Oncology reports · 2025Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimBreast cancer is a heterogenous disease characterized by complex molecular pathways that drive its progression. Despite advances in treatment strategies, the need for novel therapeutic targets remains critical. Replication factor C subunit 4 (RFC4) is an important component of the DNA replication machinery and repair pathways. Its precise regulation ensures genomic stability and its dysregulation is implicated in various cancers. However, its oncogenic role in breast cancer is unclear. Therefore, this study aimed to elucidate the biological role of RFC4 in breast cancer. MATERIALS AND
methodsBreast cancer cell lines MCF7, BT-549, and MDA-MB-231 were transfected with control and RFC4 siRNA to investigate biological functions of RFC4 in breast cancer. Cell proliferation was measured using the MTT and colony formation assays. In addition, cell cycle analysis, migration, and invasion assays were performed on RFC4-depleted breast cancer cells.
resultssiRNA-mediated RFC4 knockdown inhibited breast cancer cell proliferation and cell cycle arrest, and reduced cell migration and invasion ability.
conclusionOur findings highlight the critical role of RFC4 in breast cancer progression. The observed decrease in cell proliferation and clonogenic potential following RFC4 knockdown suggests its potential as a therapeutic target for breast cancer.
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