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Publication : Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis.

First Author  Karantza-Wadsworth V Year  2007
Journal  Genes Dev Volume  21
Issue  13 Pages  1621-35
PubMed ID  17606641 Mgi Jnum  J:122830
Mgi Id  MGI:3715577 Doi  10.1101/gad.1565707
Citation  Karantza-Wadsworth V, et al. (2007) Autophagy mitigates metabolic stress and genome damage in mammary tumorigenesis. Genes Dev 21(13):1621-35
abstractText  Autophagy is a catabolic process involving self-digestion of cellular organelles during starvation as a means of cell survival; however, if it proceeds to completion, autophagy can lead to cell death. Autophagy is also a haploinsufficient tumor suppressor mechanism for mammary tumorigenesis, as the essential autophagy regulator beclin1 is monoallelically deleted in breast carcinomas. However, the mechanism by which autophagy suppresses breast cancer remains elusive. Here we show that allelic loss of beclin1 and defective autophagy sensitized mammary epithelial cells to metabolic stress and accelerated lumen formation in mammary acini. Autophagy defects also activated the DNA damage response in vitro and in mammary tumors in vivo, promoted gene amplification, and synergized with defective apoptosis to promote mammary tumorigenesis. Therefore, we propose that autophagy limits metabolic stress to protect the genome, and that defective autophagy increases DNA damage and genomic instability that ultimately facilitate breast cancer progression.
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