Oncogenes modulate cell sensitivity to apoptosis induced by glucose deprivation

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Maya Kansara1, Michael V Berridge

  • 1Malaghan Institute of Medical Research, PO Box 7060, Wellington South, New Zealand.

Anticancer Research
|August 28, 2004
PubMed
Abstract

Insights

Oncogenes significantly impact cancer cell survival during glucose deprivation. Some oncogenes promote apoptosis, while others, like bcr-abl, offer protection, influencing cancer cell fate.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumors exhibit increased glucose uptake, making cancer cells vulnerable to glucose deprivation.
  • Investigated the role of specific oncogenes in sensitizing cells to apoptosis induced by glucose deprivation.

Purpose of the Study:

  • To determine how oncogenes influence cancer cell apoptosis under glucose-deprived conditions.
  • To explore the differential effects of various oncogenes on cell survival and growth during metabolic stress.

Main Methods:

  • Utilized oncogene-transformed 32D cells subjected to glucose deprivation with or without IL-3.
  • Measured glucose uptake using [3H]2-deoxyglucose.
  • Assessed apoptosis via AnnexinV/propidium iodide staining, cell cycle analysis, and Western blotting for MYC expression.

Main Results:

  • v-Hras, v-src, and v-abl enhanced apoptosis in the presence of IL-3 but attenuated it in its absence.
  • bcr-abl conferred significant protection against glucose deprivation-induced apoptosis for 72 hours, irrespective of IL-3.
  • bcl-2 provided mild protection in the presence of IL-3.
  • c-MYC expression correlated with sensitivity to glucose deprivation-induced apoptosis in cells with strongly transforming oncogenes.

Conclusions:

  • Oncogenes exhibit diverse effects on apoptosis during glucose deprivation, with some promoting cell death and others conferring protection.
  • The specific oncogene and cellular context (e.g., presence of IL-3) dictate the outcome of glucose deprivation on cancer cell survival.

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