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A nuclear budding mechanism in transiently arrested cells generates drug-sensitive and drug-resistant cells

Sylvia Mansilla1, Marc Bataller, José Portugal

  • 1Instituto de Biología Molecular de Barcelona, CSIC, Parc Cientific de Barcelona, Baldiri Reixach 10, E-08028 Barcelona, Spain.

Biochemical Pharmacology
|May 26, 2009
PubMed

Insights

Doxorubicin treatment induced nuclear budding in colon cancer cells, potentially eliminating DNA or creating aneuploid cells. Some resulting cells showed drug resistance, suggesting a selective advantage.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Genetics

Background:

  • HCT116 human colon carcinoma cells are a model for studying drug-induced cellular responses.
  • Doxorubicin is a common chemotherapy agent with known cytotoxic effects.

Purpose of the Study:

  • To investigate the cellular and nuclear morphological changes in HCT116 cells following doxorubicin treatment.
  • To explore the potential mechanisms and outcomes of nuclear budding in cancer cells.

Main Methods:

  • Treatment of HCT116 cells with nanomolar doxorubicin.
  • Microscopy to observe cellular and nuclear morphology.
  • Clonogenic assays to assess cell proliferation and drug resistance.
  • Protein level analysis (p53, p21(WAF1), Mos).

Main Results:

  • Doxorubicin induced transient senescence, DNA synthesis, endopolyploidization, and multinucleation without increased mitosis.
  • A novel nuclear budding process was observed, with buds potentially escaping the parent cell.
  • Some cells proliferating post-budding exhibited drug resistance, indicating selective advantage.
  • Giant cells showed inhibited p53 and increased p21(WAF1) and Mos expression.

Conclusions:

  • Nuclear budding may serve as a mechanism for DNA segregation/elimination or aneuploid cell generation.
  • The process can lead to the emergence of drug-resistant cancer cell populations.
  • This phenomenon offers insights into cancer cell adaptation and survival strategies.

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