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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Mechanisms of apoptosis by c-Myc
1The Wistar Institute, Philadelphia, Pennsylvania 19104, USA.
Abstract:
Much recent research on c-Myc has focused on how it drives apoptosis. c-Myc is widely known as a crucial regulator of cell proliferation in normal and neoplastic cells, but until relatively recently its apoptotic properties, which appear to be intrinsic, were not fully appreciated. Its death-dealing aspects have gained wide attention in part because of their potential therapeutic utility in advanced malignancy, where c-Myc is frequently deregulated and where novel modalities are badly needed. Although its exact function remains obscure, c-Myc is a transcription factor and advances have been made in characterizing target genes which may mediate its apoptotic properties. Candidate regulators and effectors are also emerging. Among recent findings are connections to the CD95/Fas and TNF pathways and roles for the tumor suppressor p19ARF and the c-Myc-interacting adaptor protein Binl in mediating cell death. In this review I summarize the data establishing a role for c-Myc in apoptosis in diverse settings and present a modified dual signal model for c-Myc function. It is proposed that c-Myc induces apoptosis through separate 'death priming' and 'death triggering' mechanisms in which 'death priming' and mitogenic signals are coordinated. Investigation of the mechanisms that underlie the triggering steps may offer new therapeutic opportunities.
Insights
The transcription factor c-Myc, known for regulating cell proliferation, also intrinsically drives apoptosis. Research reveals c-Myc
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- c-Myc is a key regulator of cell proliferation in both normal and neoplastic cells.
- Recent research highlights c-Myc's intrinsic role in inducing apoptosis, a property with therapeutic potential in malignancy.
- c-Myc deregulation is common in advanced cancers, necessitating novel therapeutic strategies.
Purpose of the Study:
- To review the evidence for c-Myc's role in apoptosis across various cellular contexts.
- To present a modified dual signal model for c-Myc-mediated apoptosis.
- To explore potential therapeutic opportunities by investigating c-Myc's cell death mechanisms.
Main Methods:
- Literature review of studies investigating c-Myc and apoptosis.
- Analysis of c-Myc's known and candidate target genes involved in cell death.
- Examination of emerging data on c-Myc interactions with apoptosis-related pathways and proteins.
Main Results:
- c-Myc actively induces apoptosis through intrinsic mechanisms.
- Connections between c-Myc, CD95/Fas and TNF pathways, p19ARF, and Bin1 in cell death are identified.
- A modified dual signal model proposes c-Myc coordinates 'death priming' and 'death triggering' with mitogenic signals.
Conclusions:
- c-Myc plays a significant role in inducing apoptosis, distinct from its proliferative functions.
- Understanding the mechanisms of c-Myc-induced cell death, particularly the 'death triggering' steps, could yield new cancer therapies.
- Further investigation into c-Myc's apoptotic pathways is crucial for developing targeted anti-cancer treatments.
Related Concept Videos
Abnormal Proliferation
Apoptosis
Caspases
The Extrinsic Apoptotic Pathway
The Intrinsic Apoptotic Pathway
Cellular Injury V: Apoptosis and Autophagy

