Document Type : Original Article
Authors
- Hamideh Kadeh 1
- Tayebeh Baranzehi 2
- Milad Mollaali 2
- Neda Maserat 2
- Mohammad-Javad Shahraki 2
- Dor Mohammad Kordi-Tamandani 2
1 Dept. Oral and Maxillofacial Pathology, Oral and Dental Disease Research Center, Faculty of Dentistry, Zahedan University of Medical Sciences, Zahedan, Iran.
2 Dept. of Biology, Faculty of Science, University of Sistan and Baluchestan, Zahedan, Iran.
Abstract
Statement of the Problem: Oral squamous cell carcinoma (OSCC) is the eighth leading cause of cancer-related death worldwide. JAK2 and STAT3 primarily influence intrinsic tumor cell behavior, and CTLA4 impacts the interplay between the tumor and the host immune system in the context of cancers. There is scarce information regarding the involvement and roles of JAK2, STAT3, and CTLA4 genes in OSCC; however, the molecular mechanisms are still unclear.
Purpose: This study examined the relationship between JAK2, STAT3, and CTLA4 gene expression levels and OSCC in a group of patients in the southeast of Iran.
Materials and Method: This cross-sectional study was conducted in which the relative gene expression levels of JAK2, STAT3, and CTLA4 were compared between 23 oral paraffin tissue blocks collected from OSCC patients and 20 fresh gingival tissues collected from healthy individuals. The Real-Time quantitative PCR (RT-qPCR) assay was employed to assess relative gene expression levels. SPSS 27 was employed to perform statistical analyses.
Results: Significant differences were found between OSCC patients and healthy individuals concerning gene expression levels of JAK2 (2.4-fold, p< 0.0001), STAT3 (2.32-fold, p< 0.0001), and CTLA4 (4.09-fold, p< 0.0001). Additionally, there were significant positive correlations among JAK2-STAT3 (0.667, p< 0.001), JAK2-CTLA4 (0.771, p< 0.001), and STAT3-CTLA4 (0.635, p= 0.001) co-expressions. Moreover, gender, age groups, and tumor locations did not significantly correlate with the expression levels of these genes (p> 0.05). Nevertheless, significant differences occurred between histopathological grades and the gene expression levels of JAK2 (p< 0.001), STAT3 (p= 0.001), and CTLA4 (p< 0.001).
Conclusion: The overexpression of JAK2, STAT3, and CTLA4 can be considered triggers for OSCC development. It may be beneficial to conduct future research on OSCC by considering downstream genes involved in the JAK2/STAT3/CTLA4 axis.
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