Abstract
Background/purpose
Heat shock factor 1 (HSF1) regulates heat shock proteins and stress-responsive genes and has been implicated in tumor progression and poor prognosis in several malignancies. However, the clinicopathological significance and biological role of HSF1 in oral squamous cell carcinoma (OSCC) remain unclear. This study investigated HSF1 expression in OSCC tissues, its association with clinicopathological parameters and survival, and its functional role in OSCC cell migration.
Materials and methods
HSF1 expression was evaluated by immunohistochemical staining in 80 OSCC specimens and 20 normal oral mucosa samples. HSF1 immunoreactivity was quantified using the labeling index (LI). Associations between HSF1 LI and clinicopathological parameters were analyzed. Kaplan–Meier survival analysis and Cox proportional hazards regression were performed. The effect of HSF1 downregulation on OSCC cell migration was examined in vitro.
Results
HSF1 expression was significantly increased in OSCC tissues compared with normal oral mucosa. Higher HSF1 LI was significantly associated with advanced T classification, nodal metastasis, and advanced clinical stage. Multivariate Cox regression analysis identified advanced T classification, positive nodal status, and high HSF1 LI as independent prognostic factors for overall survival. Patients with HSF1 LI > 53% showed increased mortality risk. In vitro experiments demonstrated that HSF1 downregulation reduced OSCC cell migration.
Conclusion
HSF1 is overexpressed in OSCC and is associated with tumor progression, advanced stage, and poor prognosis. HSF1 may also contribute to OSCC cell migration, suggesting its potential as a prognostic biomarker and therapeutic target in OSCC.
Recommended Citation
Wu, Fang-Yu; Ko, Hui-Hsin; Lin, Wen-Ren; and Cheng, Shih-Jung
(2026)
"Heat shock factor 1 promotes cell migration and predicts poor prognosis in oral squamous cell carcinoma,"
Journal of Dental Sciences: Vol. 21:
Iss.
4, Article 36.
Available at:
https://jds.ads.org.tw/journal/vol21/iss4/36
Publication Date
2026
Received Date
May 18 2026
Accepted Date
May 29 2026
Final Revision Date
May 29 2026