ArticleCellular oncology (Dordrecht, Netherlands)2016
Inactivation of the LKB1-AMPK signaling pathway does not contribute to salivary gland tumor development - a short report.
Article in Cellular oncology (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- High Mobility Group Box 1 Protein in Osteoarthritic Knee Tissue and Chondrogenic Progenitor Cells: AnCartilage · 2021Article
- Review
- Membrane-binding and activation of LKB1 by phosphatidic acid is essential for development and tumour suppression.Nature communications · 2017Article
- Silymarin and its active component silibinin act as novel therapeutic alternatives for salivary gland cancer by targeting the ERK1/2-Bim signaling cascade.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- CDKN2A-p53 mediated antitumor effect of Lupeol in head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeActivation of AMPK by the tumor suppressor LKB1 represents an essential gatekeeping step for cells under energetic stress to prevent their growth and proliferation by inhibiting mTOR activation, until the energy supply normalizes. The LKB1/AMPK pathway is frequently downregulated in various types of cancer, thereby uncoupling tumor cell growth and proliferation from energy supply. As yet, little information is available on the role of the LKB1/AMPK pathway in tumors derived from salivary gland tissues.
methodsWe performed LKB1 protein expression and AMPK and mTOR activation analyses in several salivary gland tumor types and their respective healthy control tissues using immunohistochemistry.
resultsNo significant downregulation of LKB1 expression or decreased activation of AMPK or mTOR were observed in any of the salivary gland tumors tested. In contrast, we found that the salivary gland tumors exhibited an increased rather than a decreased AMPK activation. Although the PI3K/Akt pathway was found to be activated in most of the analyzed tumor samples, the unchanged robust activity of LKB1/AMPK likely prevents (over)activation of mTOR.
conclusionIn contrast to many other types of cancer, inactivation or downregulation of the LKB1/AMPK pathway does not substantially contribute to the pathogenesis of salivary gland tumors.
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