Related Experiment Video
Updated: Jun 30, 2026
10:21
Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Cooperative interaction between c-myc and bcl-2 proto-oncogenes
A Fanidi1, E A Harrington, G I Evan
1Biochemistry of the Cell Nucleus Laboratory, Imperial Cancer Research Fund, London, UK.
Nature
|October 8, 1992
Summary
The BCL-2 protein prevents apoptosis induced by the MYC oncogene, revealing a new mechanism for how these oncogenes cooperate in cancer development and drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cellular Biology
Background:
- The BCL-2 proto-oncogene is activated in B-lymphoid tumors and works with the MYC oncogene in tumor progression.
- BCL-2's role in inhibiting apoptosis is key to its function, but its synergy with MYC is not fully understood.
- MYC is known to promote cell division (mitogenesis) and also induce programmed cell death (apoptosis).
Purpose of the Study:
- To investigate the mechanism of synergy between the BCL-2 and MYC oncogenes.
- To determine if BCL-2 protein can specifically block MYC-induced apoptosis.
- To understand the implications of this interaction in cancer and drug resistance.
Main Methods:
- Investigated the effect of BCL-2 protein expression on MYC-induced apoptosis.
- Assessed whether BCL-2 affects MYC's mitogenic function.
Main Results:
- BCL-2 protein specifically abrogates apoptosis induced by MYC.
- BCL-2 does not affect the mitogenic function of MYC.
- This interaction provides a novel mechanism for oncogene cooperation.
Conclusions:
- BCL-2 and MYC oncogenes cooperate through BCL-2's ability to inhibit MYC-induced apoptosis.
- This finding is significant for understanding carcinogenesis and the development of drug resistance in tumors.
- Identified a new pathway for oncogene cooperation with potential therapeutic implications.
Related Concept Videos
02:23Abnormal Proliferation
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
02:50Combination Therapies and Personalized Medicine
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:31The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
01:06Induced Pluripotent Stem Cells
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
Somatic cells are...