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Related Concept Videos

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...
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Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
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BRD7 is a candidate tumour suppressor gene required for p53 function.

Jarno Drost1, Fiamma Mantovani, Francesca Tocco

  • 1The Netherlands Cancer Institute, Division of Gene Regulation, Plesmanlaan 121, 1066CX, Amsterdam, The Netherlands.

Nature Cell Biology
|March 16, 2010
PubMed
Summary
This summary is machine-generated.

Bromodomain-containing 7 (BRD7) acts as a tumor suppressor by enabling p53-dependent cellular senescence. Loss of BRD7 facilitates cancer development even with functional p53, highlighting its critical role in preventing uncontrolled cell growth.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Biology

Background:

  • Oncogene-induced senescence is a crucial p53-dependent tumor suppression mechanism.
  • Many human tumors exhibit p53 mutations or pathway dysfunction, often through unknown mechanisms.
  • Understanding factors that bypass p53-mediated tumor suppression is vital for cancer therapy.

Purpose of the Study:

  • To identify novel proteins involved in p53-dependent oncogene-induced senescence.
  • To elucidate the role of BRD7 (bromodomain-containing 7) in preventing neoplastic transformation.
  • To investigate the mechanism by which BRD7 interacts with the p53 pathway.

Main Methods:

  • Analysis of BRD7 gene deletions and expression in human breast tumors.
  • Investigating the functional requirement of BRD7 in p53-mediated transcription.
  • Biochemical assays to study BRD7 interaction with p53 and p300.
  • Chromatin immunoprecipitation to assess BRD7 recruitment to target gene promoters.

Main Results:

  • BRD7 inhibition promotes neoplastic transformation in wild-type p53 cells.
  • BRD7 gene deletions and low expression correlate with wild-type p53 status in breast tumors.
  • BRD7 acts as a cofactor for p53, enhancing transcription of specific target genes.
  • BRD7 influences histone and p53 acetylation at target gene promoters.

Conclusions:

  • BRD7 is a critical tumor suppressor that functions as a p53 cofactor.
  • BRD7 is essential for the induction of p53-dependent oncogene-induced senescence.
  • BRD7 deficiency contributes to tumorigenesis by impairing p53-mediated cell cycle arrest.