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Cell cycle arrest by glucocorticoids may protect normal tissue and solid tumors from cancer therapy

Jürgen Mattern1, Markus W Büchler, Ingrid Herr

  • 1Molecular OncoSurgery, Department of Surgery, University and German Cancer Research Center (DKFZ), Heidelberg, Germany.

Cancer Biology & Therapy
|December 19, 2007
PubMed

Insights

Glucocorticoids can help cancer patients by reducing side effects but may also cause therapy resistance in solid tumors. This resistance is linked to glucocorticoid-induced cell cycle arrest, promoting tumor survival.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Glucocorticoids are used in cancer therapy for their anti-inflammatory and anti-emetic effects.
  • They exhibit pro-apoptotic properties in lymphoid cells and reduce toxicity in normal tissues.
  • Emerging evidence suggests glucocorticoids may induce therapy resistance in solid tumors.

Purpose of the Study:

  • To review the current understanding of the relationship between glucocorticoid-induced cell cycle arrest and therapy resistance in solid tumors.
  • To summarize the mechanisms by which glucocorticoids influence proliferation and survival signaling in cancer cells.

Main Methods:

  • Review of preclinical and clinical studies on glucocorticoid effects in cancer therapy.
  • Analysis of data on glucocorticoid-induced cell cycle regulation and its impact on treatment outcomes.
  • Synthesis of current knowledge on glucocorticoid signaling pathways involved in therapy resistance.

Main Results:

  • Glucocorticoids can induce reversible cell cycle arrest in malignant solid tumors.
  • Decreased proliferation rates, potentially mediated by glucocorticoids, may protect both normal tissues and solid tumors from cytotoxic agents.
  • Glucocorticoid treatment may shift cellular pathways towards survival, contributing to therapy resistance.

Conclusions:

  • Glucocorticoid-induced cell cycle arrest is a key factor in developing therapy resistance in solid tumors.
  • Understanding these mechanisms is crucial for optimizing cancer treatment strategies involving glucocorticoids.
  • Further research into glucocorticoid signaling is needed to mitigate resistance and improve patient outcomes.

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