Abstract
Mammalian target of rapamycin (mTOR) is a crucial molecule in the control of cell size and proliferation; dysregulation of the mTOR pathway is commonly found in human cancers. Many cancer-promoting kinases have been identified as regulators of mTOR activity through phosphorylation and inactivation of the TSC1-TSC2 complex. Tumor-associated macrophages (TAMs) are tumor-promoting factors in inflammation-mediated tumor development, and the signaling molecules involved in TAMs-mediated tumor angiogenesis are not well understood. Therefore, it is urgent to elucidate the cross-talk between inflammatory cells and cancers and to explore the precise pathways involved in TAMs-induced tumor angiogenesis. Recently IKKb was found to activate the mTOR pathway and to promote tumor angiogenesis through inactivation of the TSC1-TSC2 complex by phosphorylating TSC1. This finding provides critical insights into and suggests one mechanism behind inflammation-mediated tumor angiogenesis. In this extra-view, we briefly discuss the possible influence of TAMs-released proangiogenic factors on mTOR activation and propose a model of the cross-talk between tumors and TAMs in tumor angiogenesis.
Original language | English (US) |
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Pages (from-to) | 3011-3014 |
Number of pages | 4 |
Journal | Cell Cycle |
Volume | 6 |
Issue number | 24 |
DOIs | |
State | Published - Dec 15 2007 |
Keywords
- IKKβ
- Inflammation
- TAMs
- TSC1
- Tumor angiogenesis
- mTOR
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology