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- Title
THBS1 -Mediated Degradation of Collagen via the PI3K/AKT Pathway Facilitates the Metastasis and Poor Prognosis of OSCC.
- Authors
Wen, Zhihao; Zhang, Yuxiao; Wang, Xiangyao; Wu, Yaxin; Mao, Jing; Li, Qilin; Gong, Shiqiang
- Abstract
Oral squamous cell carcinoma (OSCC) is a prevalent form of malignant tumor, characterized by a persistently high incidence and mortality rate. The extracellular matrix (ECM) plays a crucial role in the initiation, progression, and diverse biological behaviors of OSCC, facilitated by mechanisms such as providing structural support, promoting cell migration and invasion, regulating cell morphology, and modulating signal transduction. This study investigated the involvement of ECM-related genes, particularly THBS1, in the prognosis and cellular behavior of OSCC. The analysis of ECM-related gene data from OSCC samples identified 165 differentially expressed genes forming two clusters with distinct prognostic outcomes. Seventeen ECM-related genes showed a significant correlation with survival. Experimental methods were employed to demonstrate the impact of THBS1 on proliferation, migration, invasion, and ECM degradation in OSCC cells. A risk-prediction model utilizing four differentially prognostic genes demonstrated significant predictive value in overall survival. THBS1 exhibited enrichment of the PI3K/AKT pathway, indicating its potential role in modulating OSCC. In conclusion, this study observed and verified that ECM-related genes, particularly THBS1, have the potential to influence the prognosis, biological behavior, and immunotherapy of OSCC. These findings hold significant implications for enhancing survival outcomes and providing guidance for precise treatment of OSCC.
- Subjects
PI3K/AKT pathway; GENE expression; SQUAMOUS cell carcinoma; SURVIVAL rate; COLLAGEN; PROGRESSION-free survival; SURVIVAL analysis (Biometry)
- Publication
International Journal of Molecular Sciences, 2023, Vol 24, Issue 17, p13312
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms241713312