title: Inactivation of the LKB1-AMPK signaling pathway does not contribute to salivary gland tumor development - a short report.
abstract: OBJECTIVE
  Activation 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.
  
  
  METHODS
  We performed LKB1 protein expression and AMPK and mTOR activation analyses in several salivary gland tumor types and their respective healthy control tissues using immunohistochemistry.
  
  
  RESULTS
  No 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.
  
  
  CONCLUSIONS
  In 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.
authors.affiliation: Molecular and Cellular Anatomy, University of Regensburg, Universitätsstr. 31, 93053, Regensburg, Germany.
authors.forename: Natascha
authors.initials: N
authors.lastname: Cidlinsky
authors.affiliation: Molecular and Cellular Anatomy, University of Regensburg, Universitätsstr. 31, 93053, Regensburg, Germany.
authors.forename: Giada
authors.initials: G
authors.lastname: Dogliotti
authors.affiliation: Department of Internal Medicine III, Hematology and Medical Oncology, University Hospital Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Pukrop
authors.affiliation: Institute for Pathology, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany.
authors.forename: Rudolf
authors.initials: R
authors.lastname: Jung
authors.affiliation: Institute for Pathology, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053, Regensburg, Germany.
authors.forename: Florian
authors.initials: F
authors.lastname: Weber
authors.affiliation: Molecular and Cellular Anatomy, University of Regensburg, Universitätsstr. 31, 93053, Regensburg, Germany. Michael.Krahn@vkl.Uni-Regensburg.de.
authors.forename: Michael P
authors.initials: MP
authors.lastname: Krahn
mesh_terms: D000091162:AMP-Activated Protein Kinase Kinases; D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D015153:Blotting, Western; D002471:Cell Transformation, Neoplastic; D015536:Down-Regulation; D006801:Humans; D007150:Immunohistochemistry; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D012468:Salivary Gland Neoplasms / Q000378:metabolism / Q000473:pathology*; D015398:Signal Transduction; D046888:Tissue Array Analysis
chemical_list: D017346:Protein Serine-Threonine Kinases; C109790:STK11 protein, human; D000091162:AMP-Activated Protein Kinase Kinases; D055372:AMP-Activated Protein Kinases
keywords: AMPK; LKB1; PI3K-pathway; Salivary gland tumor; mTOR