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Cortisol-induced SRSF3 expression promotes GR splicing, RACK1 expression and breast cancer cells migration

Erica Buoso1, Melania Ronfani1, Marilisa Galasso1

  • 1Department of Drugs Sciences, Università degli Studi di Pavia, Viale Taramelli 12/14, 27100, Pavia, Italy.

Pharmacological Research
|March 14, 2019
PubMed

Insights

High glucocorticoid receptor alpha (GRα) expression in triple-negative breast cancer (TNBC) drives therapy resistance. This study reveals GRα transcriptionally regulates RACK1, impacting cell migration and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Triple-negative breast cancer (TNBC) with high glucocorticoid receptor (GR) expression is linked to therapy resistance and poor outcomes.
  • Glucocorticoid receptor alpha (GRα) is the primary active form of GR, mediating glucocorticoid effects.
  • RACK1 (Receptor for Activated C Kinase 1) is a scaffolding protein implicated in breast cancer cell migration and invasion.

Purpose of the Study:

  • To investigate the role of GRα in regulating RACK1 expression.
  • To elucidate the mechanism by which GRα influences RACK1.
  • To explore the potential role of cortisol and SRSF3 in this pathway.

Main Methods:

  • Investigated the transcriptional regulation of RACK1 by GRα.
  • Examined the involvement of the splicing factor SRSF3.
  • Assessed the impact of cortisol on the GRα-RACK1 pathway.

Main Results:

  • Demonstrated that GRα transcriptionally regulates RACK1.
  • Identified a mechanism involving SRSF3, which promotes GRα necessary for RACK1 regulation.
  • Showed that cortisol can positively modulate this pathway.
  • Established that this pathway is crucial for breast cancer cell migration and invasion.

Conclusions:

  • Elucidated a novel mechanism of RACK1 transcriptional regulation by GRα.
  • Highlighted the critical role of SRSF3 in mediating GRα-dependent cell migration.
  • Identified a new pathway involving GRα, SRSF3, and RACK1 in TNBC progression.
  • Suggested that targeting this pathway could offer new therapeutic strategies for GR-positive TNBC.
Keywords:
Breast cancerCortisolGRRACK1SRSF3TNBC

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