Evidence map›Paper›PMID 23023215›Full record

ArticleIranian biomedical journal2012

GSK3β and CREB3 gene expression profiling in benign and malignant salivary gland tumors.

Nastaran Mohammadi Ghahhari, Hamed Mohammadi Ghahhari, Mehdi Kadivar

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Article in Iranian biomedical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Nastaran Mohammadi GhahhariDept. of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
Hamed Mohammadi GhahhariDept. of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
Mehdi KadivarDept. of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
Pasteur Institute of Iran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSalivary 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.

methodsForty 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.

resultsData 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.

conclusionGSK3β 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.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticCyclic AMP Response Element-Binding ProteinElectrophoresis, Agar GelGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansReal-Time Polymerase Chain ReactionRNA Polymerase IISalivary Gland NeoplasmsCREB3 protein, humanCyclic AMP Response Element-Binding ProteinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanRNA Polymerase IICREB3 proteinGene expression profilingglycogen synthase kinase 3 betaSalivary Gland neoplasms

Identifiers

PMID23023215
PMCPMC3629933
OpenAlexW2134729417

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