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All roads lead to mTOR: integrating inflammation and tumor angiogenesis

Dung-Fang Lee1, Mien-Chie Hung

  • 1Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.

Cell Cycle (Georgetown, Tex.)
|December 13, 2007
PubMed

Insights

Inflammation promotes cancer by activating the mammalian target of rapamycin (mTOR) pathway. IKKbeta phosphorylates TSC1, inactivating the TSC1-TSC2 complex, which drives tumor angiogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Mammalian target of rapamycin (mTOR) pathway dysregulation is common in human cancers.
  • Tumor-associated macrophages (TAMs) promote inflammation-mediated tumor development and angiogenesis.
  • Mechanisms of TAMs-induced tumor angiogenesis are not fully understood.

Purpose of the Study:

  • To elucidate the cross-talk between inflammatory cells and cancers.
  • To explore pathways involved in TAMs-induced tumor angiogenesis.
  • To understand the role of IKKbeta in mTOR activation and tumor angiogenesis.

Main Methods:

  • Investigated the role of IKKbeta in activating the mTOR pathway.
  • Examined the phosphorylation and inactivation of the TSC1-TSC2 complex by IKKbeta.
  • Proposed a model for cross-talk between tumors and TAMs in tumor angiogenesis.

Main Results:

  • IKKbeta activates the mTOR pathway.
  • IKKbeta promotes tumor angiogenesis by phosphorylating TSC1 and inactivating the TSC1-TSC2 complex.
  • This provides a mechanism for inflammation-mediated tumor angiogenesis.

Conclusions:

  • IKKbeta is a key mediator linking inflammation to mTOR activation and tumor angiogenesis.
  • Understanding TAMs-released factors influencing mTOR is crucial.
  • This study proposes a model for tumor-TAM cross-talk in angiogenesis.

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