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Cellular adaptation to nutrient deprivation: crosstalk between the mTORC1 and eIF2α signaling pathways and

Jordan C Wengrod1, Lawrence B Gardner

  • 1a Department of Biochemistry and Molecular Pharmacology ; New York University School of Medicine , New York , NY USA.

Cell Cycle (Georgetown, Tex.)
|June 4, 2015
PubMed

Insights

Tumor cells adapt to stress via autophagy, regulated by mammalian target of rapamycin complex 1 (mTORC1) and eIF2α. This review explores their roles in tumorigenesis and presents a new model of their crosstalk.

Area of Science:

  • Oncology
  • Cellular Biology
  • Molecular Biology

Background:

  • The tumor microenvironment imposes cellular stresses like hypoxia and nutrient deprivation.
  • Cells activate stress-response mechanisms, including autophagy, to survive.
  • Autophagy degrades cellular components for energy, crucial for tumor adaptation.

Purpose of the Study:

  • To review how tumor microenvironment conditions regulate mTORC1 and eIF2α signaling.
  • To examine the downstream effects of these pathways in tumorigenesis.
  • To present a novel model of crosstalk between mTORC1 and eIF2α signaling.

Main Methods:

  • Literature review of cellular stress responses in tumors.
  • Analysis of signaling pathways: mTORC1 and eIF2α.
  • Exploration of pathway crosstalk, particularly in response to amino acid deprivation.

Main Results:

  • Tumor microenvironment stresses regulate mTORC1 and eIF2α.
  • These pathways impact protein synthesis, proliferation, and autophagy.
  • Similarities and overlapping functions in stress response identified.

Conclusions:

  • mTORC1 and eIF2α are key regulators of cellular adaptation in tumors.
  • Understanding their crosstalk offers new insights into tumorigenesis.
  • A novel model highlights their interconnected roles in nutrient deprivation response.
Keywords:
PP6CautophagyeIF2αintegrated stress responsemTORC1unfolded protein response

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