Related Experiment Video

Updated: Jun 10, 2026

Monitoring Protein-RNA Interaction Dynamics In Vivo at High Temporal Resolution Using χCRAC
09:15

Monitoring Protein-RNA Interaction Dynamics In Vivo at High Temporal Resolution Using χCRAC

Published on: May 9, 2020

An emerging role for nuclear RNA-mediated responses to genotoxic stress

Roberta Busà1, Claudio Sette

  • 1Department of Public Health and Cell Biology, University of Rome Tor Vergata, Rome, Italy.

RNA Biology
|July 20, 2010
PubMed

Insights

Alternative splicing defects are crucial in cancer development. Cancer cells alter splicing factor Sam68 localization under genotoxic stress to survive, producing cancer-specific gene products.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Alternative splicing dysregulation is implicated in human cancer onset and progression.
  • Cancer cells adapt to hostile environments by modulating mRNA variants through alternative splicing.
  • Genotoxic stress from chemotherapy or irradiation significantly impacts gene splicing.

Purpose of the Study:

  • To investigate the role of splicing factor Sam68 in cancer cells' response to genotoxic stress.
  • To explore the mechanism by which cancer cells survive DNA-damaging insults via altered splicing.
  • To understand the link between chromatin conformation changes and splicing factor redistribution.

Main Methods:

  • Analysis of splicing factor expression and localization in cancer cells.
  • Investigating the impact of genotoxic stress on gene splicing patterns.
  • Studying the role of RNA-binding protein Sam68 in response to DNA-damaging agents.

Main Results:

  • Overexpressed Sam68 in tumors accumulates in nuclear foci during genotoxic stress.
  • Sam68 affects the splicing of target mRNAs in response to genotoxic stress.
  • Genotoxic drugs induce changes in chromatin conformation, guiding splicing factor redistribution.

Conclusions:

  • Subcellular redistribution of splicing factors, like Sam68, is guided by DNA-damage-induced chromatin changes.
  • This redistribution is a potential cancer cell survival mechanism against genotoxic insults.
  • Cancer cells may utilize altered splicing to express pro-survival, cancer-specific gene products.

More Related Videos

Measurements of Physiological Stress Responses in C. Elegans10:36

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Related Concept Videos

Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview
Nucleosome Remodeling02:54

Nucleosome Remodeling

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
Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
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...