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Telomeric plasmid induces human cancer cell dysfunction depending on ATM activity

Xiao-Fei Guo1, En-Hua Cao

  • 1Institute of Biophysics, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Chaoyang District, Beijing, PR China.

Cell Biochemistry and Function
|June 11, 2010
PubMed

Insights

Telomeric plasmids induce cell dysfunction and senescence by activating the ATM-p53 pathway. This study reveals how these plasmids cause telomere dysfunction, impacting cell viability and cell cycle progression.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Telomeres are crucial for chromosome stability and cellular lifespan.
  • Exogenous telomeric repeats are known to activate p53 protein.
  • The mechanism of cell dysfunction induced by telomeric plasmids remains unclear.

Purpose of the Study:

  • To investigate how telomeric plasmids induce cell dysfunction.
  • To elucidate the role of the ATM-p53 pathway in telomeric plasmid-induced effects.
  • To analyze the impact of telomeric plasmids on cell viability, senescence, and cell cycle.

Main Methods:

  • Transient transfection of human gastric cancer MGC-803 cells with a telomeric plasmid (pRST5).
  • Assessment of cell viability, senescence, and G2/M cell cycle arrest.
  • Analysis of ATM-dependent protein expression (p53, TRF1, TRF2).
  • Observation of telomere dysfunction-induced foci (TIF).

Main Results:

  • pRST5 transfection decreased cell viability by 27% and increased senescence by 62%.
  • Cells transfected with telomeric plasmids exhibited G2/M cell cycle arrest.
  • ATM-dependent upregulation of p53, TRF1, and TRF2 was observed.
  • Telomere dysfunction-induced foci (TIF) were detected in transfected cells.

Conclusions:

  • Telomeric plasmids can trigger endogenous telomere dysfunction.
  • Activation of the ATM-p53 pathway is a key mechanism in telomeric plasmid-induced cell senescence.
  • These findings provide insights into the cellular response to exogenous telomeric DNA.

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