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Updated: May 18, 2026
Ultrasonographic Evaluation of Salivary Glands for Sjogren's Syndrome: Diagnostic and Monitoring Insights
Published on: October 13, 2023
GSK3β and CREB3 gene expression profiling in benign and malignant salivary gland tumors
Nastaran Mohammadi Ghahhari1, Hamed Mohammadi Ghahhari1, Mehdi Kadivar1
1Dept. of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
Background:
Salivary gland tumors (SGT) are rare lesions with uncertain histopathology. One of the major signaling pathways that participate in the development of several tumors is protein kinase A. In this pathway, glycogen synthase kinase β (GSK3β) and cAMP responsive element binding protein (CREB3) are two genes which are supposed to be down regulated in most human tumors. The expression level of the genes was evaluated in SGT to scrutinize their possible under expression in these tumors.
Methods:
Forty eight fresh tissue samples were obtained from patients with benign and malignant SGT, including pleomorphic adenoma, warthin's tumor, mucoepidermoid carcinoma (MEC), salivary duct carcinoma and carcinoma ex pleomorphic adenoma. Eight normal samples were used as controls. Quantitative real-time PCR was used to analyze the expression level of interest genes.
Results:
Data was analyzed by statistical methods. GSK3β was downregulate in all samples and all results were statistically significant (P<0.05). CREB3 did not show a significant decrease or increase in its mRNA expression, but the results were significant in MEC and salivary duct carcinoma.
Conclusion:
GSK3β down regulation has been reported in many human tumors. This gene stimulates CREB3, inducing cell proliferation and oncogenesis. Our findings showed GSK β down regulation; however, CREB3 expression level was close to normal group. No association between CREB3 expression and inactivated GSK3β could be postulated in SGT.
Insights
Glycogen synthase kinase β (GSK3β) was downregulated in salivary gland tumors (SGT). However, cAMP responsive element binding protein (CREB3) expression remained unchanged, suggesting no direct link to GSK3β inactivation in SGT development.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Salivary gland tumors (SGT) are rare and often have unclear histopathology.
- The protein kinase A pathway is implicated in various tumor developments.
- Glycogen synthase kinase β (GSK3β) and cAMP responsive element binding protein (CREB3) are potential tumor suppressors often downregulated in human cancers.
Purpose of the Study:
- To investigate the expression levels of GSK3β and CREB3 in SGT.
- To determine if GSK3β and CREB3 are underexpressed in SGT.
- To explore the relationship between GSK3β and CREB3 in the context of SGT.
Main Methods:
- Analysis of 48 fresh SGT tissue samples (benign and malignant) and 8 normal controls.
- Utilized quantitative real-time PCR to assess gene expression levels.
- Statistical analysis was performed on the collected data.
Main Results:
- GSK3β was significantly downregulated across all SGT samples (P<0.05).
- CREB3 mRNA expression showed no significant change overall, but alterations were noted in mucoepidermoid carcinoma and salivary duct carcinoma.
- A statistically significant downregulation of GSK3β was observed in all SGT samples.
Conclusions:
- GSK3β downregulation is a consistent finding in SGT, aligning with observations in other human tumors.
- Despite GSK3β downregulation, CREB3 expression levels were comparable to normal tissues.
- No direct association between CREB3 expression and GSK3β inactivation was found in salivary gland tumors.
