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SPROUTY-2 and E-cadherin regulate reciprocally and dictate colon cancer cell tumourigenicity

A Barbáchano1, P Ordóñez-Morán, J M García

  • 1Departamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas 'Alberto Sols', Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.

Oncogene
|June 15, 2010
PubMed

Insights

SPROUTY-2 (SPRY2) is inhibited by vitamin D in colon cancer cells. SPRY2 represses E-cadherin, promoting tumor growth and suggesting SPRY2 as a therapeutic target and marker for high-grade colon cancers.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell signaling

Background:

  • SPROUTY-2 (SPRY2) is a negative regulator of receptor tyrosine kinase signaling, impacting cell growth and differentiation.
  • Vitamin D metabolites, such as 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), are known to influence cellular processes.
  • E-cadherin is a crucial cell adhesion molecule often downregulated in cancer.

Purpose of the Study:

  • To investigate the regulatory relationship between SPRY2 and E-cadherin in colon cancer.
  • To explore the role of 1,25(OH)(2)D(3) in modulating SPRY2 expression and its downstream effects.
  • To determine the clinical relevance of SPRY2 and E-cadherin expression in colon cancer patients.

Main Methods:

  • Investigated SPRY2 expression in colon cancer cells treated with 1,25(OH)(2)D(3).
  • Assessed the impact of SPRY2 on E-cadherin and epithelial-to-mesenchymal transition (EMT) markers like ZEB1.
  • Analyzed SPRY2 and E-cadherin protein levels in colon cancer cell lines, xenografts, and patient tumors.

Main Results:

  • 1,25(OH)(2)D(3) inhibits SPRY2 expression in colon cancer cells via E-cadherin-dependent and -independent pathways.
  • SPRY2 represses both basal and 1,25(OH)(2)D(3)-induced E-cadherin expression, partly through ZEB1 induction.
  • SPRY2 and E-cadherin protein levels show an inverse correlation in colon cancer cell lines, xenografts, and patient samples.
  • SPRY2 is upregulated in undifferentiated, high-grade colon tumors and at the invasive front of low-grade carcinomas.

Conclusions:

  • SPRY2 promotes colon tumorigenesis by repressing E-cadherin, likely via ZEB1 induction.
  • A reciprocal regulatory loop exists between SPRY2 and E-cadherin, influencing colon cancer cell phenotype.
  • SPRY2 is a potential biomarker for high-grade colon tumors and a target for therapeutic intervention.

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