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dc.contributor.authorGhahhari, NM
dc.contributor.authorGhahhari, HM
dc.contributor.authorKadivar, M
dc.date.accessioned2018-08-26T08:04:13Z
dc.date.available2018-08-26T08:04:13Z
dc.date.issued2012
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/49499
dc.description.abstractBackground: 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-beta. 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 upregulated 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.
dc.language.isoEnglish
dc.relation.ispartofONKOLOGIE
dc.subjectSalivary gland neoplasms
dc.subjectLKB1
dc.subjectSMAD4
dc.subjectGene expression profiling
dc.titleCould a Possible Crosstalk between AMPK and TGF-beta Signaling Pathways Be a Key Player in Benign and Malignant Salivary Gland Tumors?
dc.typeArticle
dc.citation.volume35
dc.citation.issue12
dc.citation.spage770
dc.citation.epage774
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1159/000345131


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