Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

• Autorzy: Ptak-Belowska A. , Pawlik M.W. , Krzysiek-Maczka G. , Brzozowski T. , Pawlik W.W.
• Języki publikacji: EN

Abstrakty

EN

Peroxisome proliferator-activated receptor (PPAR ) are members of the largest nuclear hormone receptor family of transcription factors (1). PPAR gamma (PPAR) plays an important role in adipogenesis, control of sensitivity to insulin, inflammation and atherosclerosis but recent studies also suggest that PPAR is involved in cell cycle withdrawal. PPAR can promote cell differentiation, exert an antiproliferative action and inhibit angiogenesis (2, 3). However, there are studies showing that activation of PPAR promotes the development of colon cancer (4). These data are in sharp contrast with studies that attribute anticancer effects to PPAR in gastrointestinal malignancies. Probably, the action of PPAR on cell cycle and proliferation depends on the cell type and presence of other stimuli that predispose cells to cancer development. Amidated and non-amidated gastrins may play an important role in the proliferation and carcinogenesis of GI cancers. It is known that gastrin peptides activate phosphorylation of Protein Kinase B (PKB/Akt) and anti-apoptotic signalling but there is little known about the link between gastrins and PPAR receptors in relation to apoptosis.

Słowa kluczowe

EN

colon cancer; transcription factor; pancreatic cancer; peroxisome proliferator-activated receptor gamma; apoptosis; adipogenesis; gastrin

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2007
• Tom: 58
• Numer: 4
• Opis fizyczny: p.793-801,fig.,ref.

Twórcy

autor

Ptak-Belowska A.

• Jagiellonian University School of Medicine, 16 Grzegorzecka Str., 31-531 Krakow, Poland

autor

Pawlik M.W.

autor

Krzysiek-Maczka G.

autor

Brzozowski T.

autor

Pawlik W.W.