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Oncogenes modulate cell sensitivity to apoptosis induced by glucose deprivation
Maya Kansara1, Michael V Berridge
1Malaghan Institute of Medical Research, PO Box 7060, Wellington South, New Zealand.
Anticancer Research
|August 28, 2004
Summary
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.