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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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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...
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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p53 gain-of-function mutations increase Cdc7-dependent replication initiation.

Arindam Datta1, Dishari Ghatak1, Sumit Das2

  • 1Cancer Biology and Inflammatory Disorder Division, CSIR-Indian Institute of Chemical Biology, Kolkata, India.

EMBO Reports
|September 10, 2017
PubMed
Summary
This summary is machine-generated.

Gain of function (GOF) mutant p53 enhances DNA replication initiation by activating Cdc7, promoting cancer cell growth. Targeting CDC7 abrogates these oncogenic phenotypes, suggesting Cdc7 as a therapeutic target for cancers with GOF mutant p53.

Keywords:
Cdc7‐Dbf4gain‐of‐functionmutant p53origin firingreplication

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • Cancer-associated p53 missense mutants exhibit gain of function (GOF), promoting tumorigenesis via altered signaling pathways.
  • The role of GOF mutant p53 in regulating DNA replication, a frequently altered cancer pathway, remains underexplored.

Purpose of the Study:

  • To investigate the role of GOF mutant p53 in regulating DNA replication initiation.
  • To explore the functional interaction between mutant p53 and the Cdc7/Dbf4 replication initiation complex.

Main Methods:

  • Investigated mutant p53's effect on Cdc7-dependent replication initiation in cancer cells.
  • Utilized in vivo and in vitro models to assess the impact of CDC7 knockdown on mutant p53-driven cancer phenotypes.
  • Correlated CDC7 expression with p53 mutational status and clinical outcomes in lung adenocarcinoma.

Main Results:

  • Mutant p53 cooperates with Myb to transactivate Cdc7 and enhances Dbf4 levels, increasing Cdc7/Dbf4 complex activity.
  • Mutant p53 cells show increased chromatin enrichment of replication factors and enhanced origin firing.
  • Knockdown of CDC7 significantly abrogated mutant p53-driven cancer phenotypes in vitro and in vivo.
  • High CDC7 expression correlates with p53 mutations and predicts poor prognosis in lung adenocarcinoma.

Conclusions:

  • Enhanced Cdc7-dependent replication initiation is a novel hallmark of p53 gain-of-function mutations in cancer.
  • Targeting the Cdc7/Dbf4 complex represents a potential therapeutic strategy for cancers harboring GOF mutant p53.