Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Al-Zoughbi, W; Pichler, M; Gorkiewicz, G; Guertl-Lackner, B; Haybaeck, J; Jahn, SW; Lackner, C; Liegl-Atzwanger, B; Popper, H; Schauer, S; Nusshold, E; Kindt, AS; Trajanoski, Z; Speicher, MR; Haemmerle, G; Zimmermann, R; Zechner, R; Vesely, PW; Hoefler, G.
Loss of adipose triglyceride lipase is associated with human cancer and induces mouse pulmonary neoplasia.
Oncotarget. 2016; 7(23):33832-33840 Doi: 10.18632/oncotarget.9418 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz

Al-Zoughbi Wael

Höfler Gerald

Vesely Paul

Co-Autor*innen der Med Uni Graz

Gorkiewicz Gregor

Gürtl-Lackner Barbara

Haybäck Johannes

Jahn Stephan

Lackner Karoline

Liegl-Atzwanger Bernadette

Nußhold Elisa

Pichler Martin

Popper Helmuth

Schauer Silvia

Speicher Michael

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Abstract:

Metabolic reprogramming is a hallmark of cancer. Understanding cancer metabolism is instrumental to devise innovative therapeutic approaches. Anabolic metabolism, including the induction of lipogenic enzymes, is a key feature of proliferating cells. Here, we report a novel tumor suppressive function for adipose triglyceride lipase (ATGL), the rate limiting enzyme in the triglyceride hydrolysis cascade.In immunohistochemical analysis, non-small cell lung cancers, pancreatic adenocarcinoma as well as leiomyosarcoma showed significantly reduced levels of ATGL protein compared to corresponding normal tissues. The ATGL gene was frequently deleted in various forms of cancers. Low levels of ATGL mRNA correlated with significantly reduced survival in patients with ovarian, breast, gastric and non-small cell lung cancers. Remarkably, pulmonary neoplasia including invasive adenocarcinoma developed spontaneously in mice lacking ATGL pointing to an important role for this lipase in controlling tumor development.Loss of ATGL, as detected in several forms of human cancer, induces spontaneous development of pulmonary neoplasia in a mouse model. Our results, therefore, suggest a novel tumor suppressor function for ATGL and contribute to the understanding of cancer metabolism. We propose to evaluate loss of ATGL protein expression for the diagnosis of malignant tumors. Finally, modulation of the lipolytic pathway may represent a novel therapeutic approach in the treatment of human cancer.

Find related publications in this database (using NLM MeSH Indexing)

Adenocarcinoma - enzymology

Adenocarcinoma - genetics

Adenocarcinoma - pathology

Adenocarcinoma of Lung -

Animals -

Biomarkers, Tumor - analysis

Biomarkers, Tumor - genetics

Cell Transformation, Neoplastic - genetics

Cell Transformation, Neoplastic - metabolism

Cell Transformation, Neoplastic - pathology

Computational Biology -

Data Mining -

Databases, Genetic -

Down-Regulation -

Gene Expression Regulation, Enzymologic -

Gene Expression Regulation, Neoplastic -

Genetic Predisposition to Disease -

Humans -

Lipase - analysis

Lipase - deficiency

Lipase - genetics

Lipolysis -

Lung Neoplasms - enzymology

Lung Neoplasms - genetics

Lung Neoplasms - pathology

Mice, Inbred C57BL -

Mice, Knockout -

Neoplasms - enzymology

Neoplasms - genetics

Neoplasms - pathology

Phenotype -

Find related publications in this database (Keywords)

adipose triglyceride lipase

cancer metabolism

lipolysis

diagnostic marker

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