期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-05388-x
关键词
-
资金
- Wellcome Trust [095317/Z/11/Z]
- UK Dementia Research Institute
- Alzheimer's Research UK
- Alzheimer's Society
- Sackler Foundation [RG70550]
- NIHR Biomedical Research Unit in Dementia at Addenbrooke's Hospital
- Treat PolyQ project (European community's Seventh Framework Programme) [264508]
- Romanian grant of Ministery of Research and Innovation CNCS-UEFISCDI within PNCDI III [PN-III-P1-1.1-PD-2016-1291]
- MRC
- [100140/Z/12/Z]
- MRC [UKDRI-2002] Funding Source: UKRI
Contact inhibition enables noncancerous cells to cease proliferation and growth when they contact each other. This characteristic is lost when cells undergo malignant transformation, leading to uncontrolled proliferation and solid tumor formation. Here we report that autophagy is compromised in contact-inhibited cells in 2D or 3D-soft extracellular matrix cultures. In such cells, YAP/TAZ fail to co-transcriptionally regulate the expression of myosin-II genes, resulting in the loss of F-actin stress fibers, which impairs autophagosome formation. The decreased proliferation resulting from contact inhibition is partly autophagy-dependent, as is their increased sensitivity to hypoxia and glucose starvation. These findings define how mechanically repressed YAP/TAZ activity impacts autophagy to contribute to core phenotypes resulting from high cell confluence that are lost in various cancers.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据