期刊
AUTOPHAGY
卷 12, 期 9, 页码 1679-1680出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2016.1203487
关键词
autophagy; cell motility; focal adhesion; metastasis; paxillin; SRC
类别
资金
- NATIONAL CANCER INSTITUTE [R01CA162405, T32CA009594] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007281] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA162405, T32 CA009594] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007281] Funding Source: Medline
Metastasis requires tumor cells to overcome a series of challenges to successfully travel to and colonize new microenvironments. As an adaptive (or maladaptive) response to stress, macroautophagy/autophagy has garnered increasing interest with respect to cancer metastasis, supported by clinical observations of increased autophagic flux in distant metastases relative to primary tumors. Recently, we identified a new role for autophagy in tumor cell motility through the turnover of focal adhesions, large multi-protein structures that link extracellular matrix-bound integrins to the cytoskeleton. The disassembly of focal adhesions at the cell rear is critical to forward movement and successful migration/invasion. We demonstrated that the focal adhesion protein PXN (paxillin), which serves as a crucial scaffolding and signal integrator, binds directly to LC3B through a conserved LC3-interacting region (LIR) motif to stimulate focal adhesion disassembly and metastasis and that this interaction is further promoted by oncogenic SRC.
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