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Three steps to the immortality of cancer cells: senescence, polyploidy and self-renewal

Jekaterina Erenpreisa1, Mark S Cragg

  • 1Latvian Biomedical Research & Study Centre, Riga LV-1047, Latvia. katrina@biomed.lu.lv.

Cancer Cell International
|September 13, 2013
PubMed

Insights

Cancer cells develop resistance to DNA damaging treatments through a life-cycle process involving senescence, polyploidy, and stemness. This programmed response rejuvenates cells, enabling survival and self-renewal after genotoxic stress.

Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Metastatic cancer often resists DNA damaging treatments due to acquired resistance.
  • Tumor cells exhibit both senescence and stemness in response to genotoxic stress, a phenomenon poorly understood.
  • Cellular senescence, typically a terminal fate, is reversible in a subset of polyploid cancer cells post-DNA damage.

Purpose of the Study:

  • To investigate the biological significance and molecular regulation of senescence and stemness in response to DNA damaging treatments.
  • To explore the link between reversible polyploidy, senescence, and stemness in overcoming genotoxic insults.
  • To elucidate the role of senescence in rejuvenating cancer cells and conferring resistance.

Main Methods:

  • Analysis of polyploid cancer cells induced by DNA damage.
  • Investigation of the relationship between senescence, autophagy, and stemness phenotypes.
  • Study of de-polyploidisation and its effect on cell self-renewal potential.

Main Results:

  • Overcoming genotoxic insults is linked to reversible polyploidy and a stemness phenotype.
  • Senescence and autophagy are integral to the self-renewal capacity of surviving cells after de-polyploidisation.
  • Senescence appears necessary for rejuvenating cancer cells post-genotoxic treatment.

Conclusions:

  • Genotoxic resistance in cancer may involve a programmed life-cycle process uniting senescence, polyploidy, and stemness.
  • Reversible polyploidy and subsequent de-polyploidisation contribute to cancer cell stemness and survival.
  • Senescence plays a paradoxical role in promoting cancer cell rejuvenation and resistance.

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