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Updated: Jan 23, 2026

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
Role of PDGF-BB in Oral Squamous Cell Carcinoma through PI3/AKT/mTOR Pathway: An Integrated Computational and
Georgia Benitha J1, Pratibha Ramani2, Selvaraj Jayaraman3
1Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai, India.
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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