Oncogenic Potential of Replication Factor C Subunit 4: Correlations with Tumor Progression and Assessment of Potential Inhibitors

Replication Factor C Subunit 4 (RFC4), an oncogene implicated in many human cancers, has yet to be extensively studied in many cancer types to determine its expression patterns and tumor tissue function. Various bioinformatics tools were used to analyze RFC4 as a potential oncogene and therapeutic t...

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Veröffentlicht in:Pharmaceuticals (Basel, Switzerland) Switzerland), 2024-01, Vol.17 (2), p.152
Hauptverfasser: Alaa Eldeen, Muhammad, Mamdouh, Farag, Abdulsahib, Waleed K, Eid, Refaat A, Alhanshani, Ahmad A, Shati, Ayed A, Alqahtani, Youssef A, Alshehri, Mohammed A, Samir A Zaki, Mohamed, Soltan, Mohamed A, Noreldin, Ahmed E
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Sprache:eng
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Zusammenfassung:Replication Factor C Subunit 4 (RFC4), an oncogene implicated in many human cancers, has yet to be extensively studied in many cancer types to determine its expression patterns and tumor tissue function. Various bioinformatics tools were used to analyze RFC4 as a potential oncogene and therapeutic target across many cancers. We first examined RFC4 expression levels in several human tumor types to determine relationships with tumor grade, stage, metastasis, and patient survival. We also examined RFC4's genetic changes, epigenetic methylation, and effect on tumor microenvironment (TME) immune cell infiltration. We also analyzed RFC4's connections with immunological checkpoints to identify potential molecular pathways involved in carcinogenesis. Our findings show that RFC4 is upregulated in several tumor types and associated with poor prognoses in many human cancers. This study shows that RFC4 significantly affects the tumor immunological microenvironment, specifically immune cell populations. Finally, we screened for RFC4-inhibiting pharmacological compounds with anti-cancer potential. This study fully elucidates RFC4's carcinogenic activities, emphasizing its potential as a prognostic biomarker and a target for anti-cancer therapy.
ISSN:1424-8247
1424-8247
DOI:10.3390/ph17020152