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Glucocorticoids suppress renal cell carcinoma progression by enhancing Na,K-ATPase beta-1 subunit expression

Thu P Huynh1, Sonali P Barwe2, Seung J Lee2

  • 1Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America; Nemours Center for Childhood Cancer Research, A. I. DuPont Hospital for Children, Wilmington, Delaware, United States of America.

Plos One
|April 4, 2015
PubMed

Insights

Glucocorticoids enhance cancer cell-cell adhesion by increasing Na,K-ATPase beta-subunit isoform 1 (NaK-β1) expression. This mechanism may improve outcomes for renal cell carcinoma (RCC) patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Glucocorticoids are used in cancer therapy, but their mechanisms of action are not fully understood.
  • Na,K-ATPase beta-subunit isoform 1 (NaK-β1) is a cell adhesion molecule downregulated during epithelial-to-mesenchymal transition (EMT) in cancer progression.
  • EMT is a key event in cancer metastasis.

Purpose of the Study:

  • To identify small molecules that upregulate NaK-β1 expression in cancer cells.
  • To investigate the role of NaK-β1 in mediating the anti-cancer effects of glucocorticoids.
  • To evaluate the therapeutic potential of NaK-β1-upregulating compounds in renal cell carcinoma (RCC).

Main Methods:

  • High-throughput screening to identify NaK-β1-upregulating compounds.
  • In vitro validation using specific glucocorticoids (triamcinolone, dexamethasone, fluorometholone) on RCC cells.
  • Assessment of cell-cell adhesion, motility, invasiveness, and EMT markers.
  • In vivo studies using RCC xenografts (subcutaneous and orthotopic models).

Main Results:

  • Glucocorticoid-related compounds were identified as NaK-β1 expression enhancers.
  • Triamcinolone, dexamethasone, and fluorometholone increased cell surface NaK-β1, enhanced cell adhesion, and reduced motility/invasiveness in RCC cells.
  • These effects were confirmed to be mediated by NaK-β1 upregulation.
  • Compounds reduced tumor growth and local invasiveness in RCC xenograft models.

Conclusions:

  • Glucocorticoids upregulate NaK-β1 expression, enhancing cell-cell adhesion and suppressing cancer progression.
  • Targeting NaK-β1 with glucocorticoids shows therapeutic promise for renal cell carcinoma (RCC).
  • Augmenting NaK-β1 function via glucocorticoids may improve clinical outcomes for RCC patients.

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