c-myc induces autophagy in rat 3Y1 fibroblast cells.

Abstract:

:The proto-oncogene c-myc is a multifunctional gene that regulates cell division, cell growth, and apoptosis. Here we report a new function of c-myc: induction of autophagy. Autophagy is a bulk degradation system for intracellular proteins. Autophagy proceeds with characteristic morphologies, which begins with the formation of a double-membrane structure called the autophagosome surrounding a portion of the cytoplasm, after which its outer membrane then fuses with the lysosomal membrane to become an autolysosome. Autophagosomes and autolysosomes are generally called autophagic vacuoles. When c-Myc protein was overexpressed in rat 3Y1 fibroblasts or when the chimeric protein c-MycER was activated by estrogen, the number of autophagic vacuoles in cells increased significantly. The formation of autophagic vacuoles induced by c-Myc was completely blocked by a specific inhibitor of autophagosome formation, 3-methyladenine. A c-Myc mutant lacking Myc Box II induced neither apoptosis nor oncogenic transformation, but still stimulated autophagy. An inhibitor of caspases suppressed apoptosis but not autophagy. These results suggest that the autophagy caused by c-myc is not due to the apoptosis or tumorigenesis induced by c-myc. Taken together, our results suggest that the induction of autophagy is a novel function of c-myc.

journal_name

Cell Struct Funct

authors

Tsuneoka M,Umata T,Kimura H,Koda Y,Nakajima M,Kosai K,Takahashi T,Takahashi Y,Yamamoto A

doi

10.1247/csf.28.195

keywords:

subject

Has Abstract

pub_date

2003-06-01 00:00:00

pages

195-204

issue

3

eissn

0386-7196

issn

1347-3700

journal_volume

28

pub_type

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