Document Type : Research Articles
Authors
1
Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, India.
2
Department of Oral and Maxillofacial Pathology, Priyadarshini Dental College and Hospitals, India.
3
Department of Oral Pathology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, India.
4
Department of Biochemistry, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.
5
Department of Oral and Maxillofacial Pathology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, Tamil Nadu, India.
Abstract
Objective: This study investigates the role of PDGF-BB in oral squamous cell carcinoma (OSCC) and its impact on the PI3K/AKT/mTOR pathway. The goal is to elucidate the expression levels analysis of PDGF-BB and signaling molecules in OSCC pathogenesis, potentially identifying novel biomarkers or therapeutic targets. Methods: A combined approach involving in silico and experimental methods was employed. Protein sequence data for PDGF-BB were obtained from UniProt, and protein-protein interactions were analyzed using STRING to visualize PDGF-BB’s network. Pathway enrichment analysis was conducted via PANTHER to identify relevant signaling pathways. The study included 30 OSCC patients and 30 matched healthy controls. Serum PDGF-BB protein levels were quantified using enzyme-linked immunosorbent assay (ELISA), while mRNA expression of PI3K, AKT, and mTOR was measured in OSCC and adjacent non-tumor tissues using quantitative real-time PCR (RT-qPCR). Results: Pathway analysis identified 12 significant signaling pathways associated with PDGF-BB, with the PI3K/AKT/mTOR pathway chosen for validation due to its relevance in cancer-related signaling. STRING analysis confirmed PDGF-BB’s interaction with this pathway. ELISA revealed significantly elevated serum PDGF-BB levels in OSCC patients (3.44 ng/mL) compared to controls (1.38 ng/mL, p < 0.05). RT-qPCR demonstrated significant upregulation of PI3K, AKT, and mTOR mRNA in OSCC tissues, with fold changes of 1.93, 2.1, and 1.9, respectively, relative to adjacent non-tumor tissues. Conclusion: PDGF-BB is significantly upregulated in OSCC and likely contributes to OSCC progression by activating the PI3K/AKT/mTOR pathway. These findings highlight PDGF-BB’s potential as a biomarker and therapeutic target in OSCC. Targeted therapies aimed at disrupting PDGF-BB and PI3K/AKT/mTOR signaling may improve OSCC outcomes, offering a promising avenue for future research and clinical applications.
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