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Table of Contents
35, No. 12, 2012
Issue release date: December 2012
Section title: Original Article · Originalarbeit
Onkologie 2012;35:770–774
(DOI:10.1159/000345131)

Could a Possible Crosstalk between AMPK and TGF-β Signaling Pathways Be a Key Player in Benign and Malignant Salivary Gland Tumors?

Ghahhari N.M.a · Ghahhari H.M.b · Kadivar M.a
aDepartment of Biochemistry, Pasteur Institute of Iran, Tehran, bDepartment of Otorhinolaryngology and Head and Neck Surgery, Imam Reza Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
email Corresponding Author

Mehdi Kadivar, M.Sc., Ph.D.

Department of Biochemistry

Pasteur Institute of Iran

No. 69, Pasteur Ave, Tehran-13164, Iran

kadivar@pasteur.ac.ir

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Abstract

Background: Salivary gland tumors (SGTs) are known for their specific heterogeneity and ambiguous outcome for the affected patients. The LKB1 and SMAD4 genes are pivotal components of important signaling pathways, including AMPK and TGF-β. To our knowledge, no study has reported an association between the expression levels of these genes in SGTs. The expression levels of LKB1 and SMAD4 were evaluated to clarify their possible crosstalk in SGTs. Materials and Methods: A total of 50 fresh tissue specimens were obtained from patients with SGTs, including pleomorphic adenoma (PA), Warthin’s tumor (WT), intermediate grade mucoepidermoid carcinoma (MEC), salivary duct carcinoma (SDC), and carcinoma ex pleomorphic adenoma (CexPA), as well as 8 normal samples. Quantitative real-time polymerase chain reaction was performed for all samples with specific primers. Results: Data were analyzed using statistical methods. PA, WT, MEC, and SDC showed a significant decrease in LKB1 levels, but the gene was up-regulated in CexPA. SMAD4 was overexpressed in all samples. Conclusion: The results suggest a possible link between downregulation of LKB1 and overexpression of SMAD4 in SGTs. LKB1 depletion leads to upregulation of SMAD4, promoting epithelial-mesenchymal transition in tumor cells. Therefore, LKB1 and SMAD4 could be key players in inducing tumor heterogeneity in SGTs.


Article / Publication Details

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Abstract of Original Article · Originalarbeit

Published online: November 20, 2012
Issue release date: December 2012

ISSN: 2296-5270 (Print)
eISSN: 2296-5262 (Online)

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