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Related Concept Videos

Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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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 Intrinsic Apoptotic Pathway01:31

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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...
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Interaction between APC and Fen1 during breast carcinogenesis.

Satya Narayan1, Aruna S Jaiswal2, Brian K Law3

  • 1Department of Anatomy and Cell Biology, University of Florida, Gainesville, FL 32610, United States.

DNA Repair
|April 19, 2016
PubMed
Summary

Aberrant DNA repair, specifically base excision repair (BER), is linked to breast cancer. The interaction between adenomatous polyposis coli (APC) and flap endonuclease 1 (Fen1) proteins may increase cancer risk.

Keywords:
Adenomatous polyposis coliBase excision repairBreast cancer developmentEnvironmental carcinogensFlap endonuclease 1Mortality

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Aberrant DNA base excision repair (BER) is implicated in malignant transformation.
  • Inter-individual variations in DNA repair capacity influence breast cancer risk.
  • Adenomatous polyposis coli (APC) and flap endonuclease 1 (Fen1) are key proteins in BER.

Purpose of the Study:

  • To review emerging evidence on the novel mechanisms by which APC and Fen1 promote breast cancer development.
  • To investigate the role of APC and Fen1 interaction in breast cancer susceptibility.
  • To explore the potential of assessing individual DNA repair capability and breast cancer risk through genetic screening.

Main Methods:

  • Review of emerging evidence on APC and Fen1 function in breast cancer.
  • Analysis of APC and Fen1 expression and interaction in breast tumors versus normal cells.
  • Investigation of the link between abrogation of long-patch BER (LP-BER) and carcinogen-induced cell transformation.

Main Results:

  • APC and Fen1 expression and interaction are increased in breast tumors.
  • APC interacts with and inhibits Fen1 activity in Pol-β-directed LP-BER.
  • Abrogation of LP-BER is associated with carcinogen-induced transformation of breast epithelial cells.
  • Carcinogens increase APC and Fen1 expression in various cell types.
  • Inactivation of APC and Fen1 tumor suppressor functions occurs through their interaction, potentially increasing breast cancer susceptibility.
  • Increased APC and Fen1 interaction may result from polymorphic or mutational variations.

Conclusions:

  • The interaction between APC and Fen1 may serve as a susceptibility factor for breast cancer.
  • Screening for APC and Fen1 variations and their interaction could assess individual DNA repair capability and breast cancer risk.
  • Reducing exposure to carcinogens may lower breast cancer risk for susceptible individuals.
  • Understanding APC and Fen1 interaction can inform the development of targeted chemopreventive and chemotherapeutic agents.