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PMID: 10625637 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Distinct classes of phosphatidylinositol 3'-kinases are involved in signaling pathways that control macroautophagy in HT-29 cells.

The Journal of biological chemistry ·Vol. 275 ·No. 2 ·2000-01-14 ·Pages 992-8

Petiot A, Ogier-Denis E, Blommaart EF, Meijer AJ, Codogno P

Abstract

3-Methyladenine which stops macroautophagy at the sequestration step in mammalian cells also inhibits the phosphoinositide 3-kinase (PI3K) activity raising the possibility that PI3K signaling controls the macroautophagic pathway (Blommaart, E. F. C., Krause, U., Schellens, J. P. M., Vreeling-Sindelárová, H., and Meijer, A. J. (1997) Eur. J. Biochem. 243, 240-246). The aim of this study was to identify PI3Ks involved in the control of macroautophagic sequestration in human colon cancer HT-29 cells. An increase of class I PI3K products (phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 3,4,5-triphosphate) caused by either feeding cells with synthetic lipids (dipalmitoyl phosphatidylinositol 3, 4-bisphosphate and dipalmitoyl phosphatidylinositol 3,4, 5-triphosphate) or by stimulating the enzymatic activity by interleukin-13 reduced macroautophagy. In contrast, an increase in the class III PI3K product (phosphatidylinositol 3-phosphate), either by feeding cells with a synthetic lipid or by overexpressing the p150 adaptor, stimulates macroautophagy. Transfection of a specific class III PI3K antisense oligonucleotide greatly inhibited the rate of macroautophagy. In accordance with a role of class III PI3K, wortmannin (an inhibitor of PI3Ks) inhibits macroautophagic sequestration and protein degradation in the low nanomolar range (IC(50) 5-15 nM). Further in vitro enzymatic assay showed that 3-methyladenine inhibits the class III PI3K activity. Dipalmitoyl phosphatidylinositol 3-phosphate supplementation or p150 overexpression rescued the macroautophagic pathway in HT-29 cells overexpressing a GTPase-deficient mutant of the Galpha(i3) protein suggesting that both class III PI3K and trimeric G(i3) protein signaling are required in the control macroautophagy in HT-29 cells. In conclusion, our results demonstrate that distinct classes of PI3K control the macroautophagic pathway in opposite directions. The roles of PI3Ks in macroautophagy are discussed in the context of membrane recycling.

MeSH Terms
Adenocarcinoma Androstadienes/pharmacology Autophagy/drug effects,physiology Chromones/pharmacology Colonic Neoplasms Enzyme Inhibitors/pharmacology Homeostasis Humans Isoenzymes/genetics,metabolism Kinetics L-Lactate Dehydrogenase/analysis Morpholines/pharmacology Phosphatidylinositol 3-Kinases/genetics,metabolism Phosphatidylinositol Phosphates/metabolism,pharmacology Protein Serine-Threonine Kinases Proto-Oncogene Proteins/metabolism Proto-Oncogene Proteins c-akt Reverse Transcriptase Polymerase Chain Reaction Signal Transduction/physiology Tumor Cells, Cultured Wortmannin
Chemicals
Androstadienes Chromones Enzyme Inhibitors Isoenzymes Morpholines Phosphatidylinositol Phosphates Proto-Oncogene Proteins 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one L-Lactate Dehydrogenase Protein Serine-Threonine Kinases Proto-Oncogene Proteins c-akt Wortmannin
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Petiot A
INSERM U504, Glycobiologie et Signalisation Cellulaire, 16 avenue Paul-Vaillant-Couturier, 94807 Villejuif, Cedex, France.
Ogier-Denis E
Blommaart E F
Meijer A J
Codogno P
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
2000-01-14
Pages
992-8
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
Corrections
ErratumIn
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