Action of Myc in vivo - proliferation and apoptosis

S Pelengaris1, B Rudolph, T Littlewood

  • 1Biological Sciences, University of Warwick, Coventry, CV4 7AL, UK. cjpy@dna.bio.warwick.ac.uk.

Insights

Oncogenes like Myc can drive cell growth and death. The balance between these processes is key to tumor development and persistence, as shown in new mouse studies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Dominant oncogenes encode proteins that regulate cell proliferation and apoptosis.
  • Dysregulation of these processes is a hallmark of cancer.
  • The balance between oncogene-driven proliferation and apoptosis is critical in tumorigenesis.

Purpose of the Study:

  • To investigate the role of the proliferation-apoptosis balance in Myc-induced carcinogenesis.
  • To understand how this balance influences tumor initiation and maintenance.

Main Methods:

  • Utilizing transgenic mouse models.
  • Employing an ectopically regulatable Myc gene or protein.
  • Analyzing the interplay between Myc expression, cell proliferation, and apoptosis.

Main Results:

  • Demonstrated that the balance between oncogene-induced proliferation and apoptosis is a critical determinant in tumor development.
  • Highlighted the significance of this balance in both the initiation and maintenance phases of carcinogenesis.
  • Provided insights into Myc's role in cancer through its influence on cell fate.

Conclusions:

  • The balance between cell proliferation and apoptosis is a crucial factor in Myc-induced cancer.
  • Modulating this balance could be a therapeutic strategy for cancer treatment.
  • Further research in this area is warranted to fully elucidate oncogene-driven tumorigenesis.

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Abnormal Proliferation02:23

Abnormal 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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Intrinsic Apoptotic Pathway01:31

The 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...
Induced Pluripotent Stem Cells01:06

Induced 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...