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Published on: January 22, 2019

Interleukin-6-independent expression of glucocorticoid receptor is upregulated by triptolide in multiple myeloma

Min Yang1, Jia-Kun Shen, Jian Huang

  • 1Department of Hematology, The First Affiliated Hospital, Institute of Hematology, Zhejiang University, School of Medicine, Zhejiang Province, People's Republic of China.

Leukemia & Lymphoma
|March 31, 2009
PubMed

Insights

Triptolide enhances dexamethasone efficacy in multiple myeloma by increasing phosphorylated glucocorticoid receptors. This combination therapy overcomes resistance, even when growth factors like interleukin-6 are present.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Glucocorticoids are standard chemotherapy for multiple myeloma.
  • Drug resistance often stems from reduced glucocorticoid receptor expression in cancer cells.

Purpose of the Study:

  • To investigate the role of glucocorticoid receptor expression in multiple myeloma drug resistance.
  • To evaluate the effect of triptolide on glucocorticoid receptor activity and dexamethasone sensitivity.

Main Methods:

  • Examined glucocorticoid receptor expression in dexamethasone-sensitive and resistant multiple myeloma cell lines.
  • Assessed the impact of triptolide on phosphorylated glucocorticoid receptor levels.
  • Tested the combined efficacy of triptolide and dexamethasone, with and without interleukin-6.

Main Results:

  • Triptolide increased the phosphorylation of the glucocorticoid receptor.
  • Triptolide potentiated the growth-inhibitory effects of dexamethasone.
  • Interleukin-6 could not block the synergistic effects of triptolide and dexamethasone.

Conclusions:

  • Triptolide can overcome dexamethasone resistance in multiple myeloma by enhancing glucocorticoid receptor signaling.
  • The combination of triptolide and dexamethasone represents a potential therapeutic strategy for resistant multiple myeloma.
  • Targeting glucocorticoid receptor phosphorylation offers a novel approach to combatting chemotherapy resistance.

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