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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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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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DNA Damage Can Stall the Cell Cycle02:37

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Overview of DNA Repair02:25

Overview of DNA Repair

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Nucleosome Remodeling02:54

Nucleosome Remodeling

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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
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Related Experiment Video

Updated: May 10, 2025

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
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Interplay Between the Cytoskeleton and DNA Damage Response in Cancer Progression.

Clarissa Esmeralda Halim1,2, Shuo Deng1,2, Karen Carmelina Crasta1,3

  • 1Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.

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Summary

The cytoskeleton plays a crucial role in DNA damage response (DDR) pathways, influencing cancer cell survival and death. Targeting the cytoskeleton alongside DDR could enhance cancer therapies.

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DNA damage responsecancercytoskeletonhomologous recombinationintermediate filamentsmicrofilamentsmicrotubulesnon-homologous end joiningtherapeutics

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Oncology

Background:

  • DNA damage is a key driver of cancer development and progression.
  • DNA damage response (DDR) pathways dictate cell fate after DNA damage, either promoting repair or cell death.
  • Cytoskeletal dynamics are increasingly recognized as critical regulators of DDR pathway function.

Purpose of the Study:

  • To review the intricate roles of cytoskeletal proteins in DNA damage response pathways within cancer cells.
  • To highlight the often-overlooked involvement of the cytoskeleton in DDR and its implications for cancer therapy.
  • To explore the potential of combining cytoskeleton-targeting agents with DDR inhibitors for improved cancer treatment.

Main Methods:

  • Literature review of existing research on cytoskeleton and DNA damage response.
  • Analysis of the involvement of microfilaments, intermediate filaments, and microtubules in DDR pathways.
  • Discussion of specific DDR pathways including non-homologous end joining (NHEJ), homologous recombination (HR), base excision repair (BER), and nucleotide excision repair (NER).

Main Results:

  • Cytoskeletal proteins are integral to DDR, involved in recruiting repair molecules and facilitating DNA mobility.
  • The cytoskeleton influences the efficacy of various DDR pathways critical for cancer cell survival.
  • The interplay between cytoskeleton and DDR is crucial for determining cancer cell fate following DNA damage induction.

Conclusions:

  • The cytoskeleton's role in DDR is essential but frequently neglected in cancer research and therapeutic strategies.
  • Exploiting the cytoskeleton-DDR axis offers novel avenues for developing more effective cancer therapies.
  • Synergistic strategies combining DDR inhibitors and cytoskeleton-targeting agents hold promise for cancer treatment.