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

2012-11-20T00:00:00Z (GMT) by Ghahhari N.M. Ghahhari H.M. Kadivar M.
<b><i>Background: </i></b>Salivary gland tumors (SGTs) are known for their specific heterogeneity and ambiguous outcome for the affected patients. The <i>LKB1 </i>and <i>SMAD4 </i>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 <i>LKB1 </i>and <i>SMAD4 </i>were evaluated to clarify their possible crosstalk in SGTs. <b><i>Materials and Methods: </i></b>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. <b><i>Results: </i></b>Data were analyzed using statistical methods. PA, WT, MEC, and SDC showed a significant decrease in <i>LKB1 </i>levels, but the gene was up-regulated in CexPA. <i>SMAD4 </i>was overexpressed in all samples. <b><i>Conclusion: </i></b>The results suggest a possible link between downregulation of <i>LKB1 </i>and overexpression of <i>SMAD4 </i>in SGTs. <i>LKB1 </i>depletion leads to upregulation of <i>SMAD4</i>, promoting epithelial-mesenchymal transition in tumor cells. Therefore, <i>LKB1 </i>and <i>SMAD4 </i>could be key players in inducing tumor heterogeneity in SGTs.