Abstract 450P
Background
Head and neck squamous cell carcinoma (HNSCC) are a significant health concern due to its high incidence and mortality rates. The gene Replication Factor C subunit 5 (RFC5), which is essential for DNA replication, encodes the smallest subunit of the replication factor C complex. RFC5 has been found to promote cellular proliferation, migration, and invasion, indicating its involvement in the development of tumors in various cancer types. However, its oncogenic role in HNSCC remains unclear. This study aims to investigate the clinicopathological correlation and prognostic value of RFC5 expression in HNSCC.
Methods
Real-time PCR, western blotting, and immunohistochemistry (IHC) were employed to assess RFC5 mRNA and protein expression in 68 HNSCC tissues and paired non-tumor tissues. Survival analysis was conducted using the Kaplan-Meier plotter. Additionally, we explored RFC5 expression and its relationship to clinicopathological characteristics and immune gene regulators using the TCGA-HNSCC dataset. RFC5 functional analysis was performed using bioinformatics.
Results
The levels of RFC5 mRNA and protein were significantly higher in HNSCC tissues compared to non-tumor tissues. Elevated RFC5 expression was associated with advanced clinicopathological features and lower overall survival rates in HNSCC patients. Functional enrichment analysis indicated that RFC5 is associated with DNA replication, HNSCC tumorigenesis, and progression, highlighting its potential role in cancer development.
Conclusions
The dysregulated expression of RFC5 in HNSCC underscores its significant role in the disease's development. RFC5 has potential as both a prognostic biomarker and a therapeutic target in HNSCC, offering new perspectives for improving patient outcomes. However, further research is urgently needed to confirm these findings and fully explore the therapeutic potential of targeting RFC5 in HNSCC.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.