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Selenite-induced apoptosis and autophagy in colon cancer cells

Věra Králová1, Soňa Benešová, Miroslav Cervinka

  • 1Department of Medical Biology and Genetics, Charles University in Prague, Faculty of Medicine in Hradec Kralove, Simkova 870, 500 38 Hradec Kralove, Czech Republic.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|December 28, 2011
PubMed

Insights

Sodium selenite (Se) induces stress in colon cancer cells, affecting apoptosis and autophagy. The absence of p53 alters these responses, impacting cell death pathways and signaling.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Death Mechanisms

Background:

  • Sodium selenite (Se) is known to induce stress responses and cell death, including apoptosis and autophagy, in cancer cells.
  • The tumor suppressor protein p53 plays a critical role in apoptosis, but its role in autophagy is complex and context-dependent.
  • Previous studies indicated differences in Se-induced growth inhibition and apoptosis in colon cancer cells with functional versus deleted p53.

Purpose of the Study:

  • To investigate the detailed mechanisms, relationship, and crosstalk between apoptosis and autophagy in Se-treated HCT-116 colon cancer cells with different p53 statuses.
  • To elucidate how the absence of p53 influences Se-induced stress responses and cell death pathways in colon cancer.

Main Methods:

  • Comparison of Se-treated HCT-116 cells (functional p53) and HCT-116-p53KO cells (deleted p53).
  • Analysis of differential activation of MAP kinases (p38 and JNK).
  • Investigation of the involvement of mTOR and PI3K signaling pathways in apoptosis and autophagy.

Main Results:

  • The absence of p53 in colon cancer cells alters the patterns of response to Se-induced stress.
  • Differential activation of MAP kinases was observed: p38 in HCT-116 and JNK in HCT-116-p53KO cells, influencing apoptosis and autophagy.
  • Deletion of p53 appears to lead to increased cellular instability and delayed decision-making regarding apoptosis versus autophagy, potentially resulting in simultaneous activation.

Conclusions:

  • p53 status significantly modulates the cellular response to sodium selenite in colon cancer, affecting the balance between apoptosis and autophagy.
  • The study highlights the dichotomous role of p53 in regulating cell death pathways and signaling in response to chemotherapeutic stress.
  • Understanding these p53-dependent mechanisms is crucial for developing targeted therapies for colon cancer.

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