A potential clinical significance of DAB2IP and SPRY2 transcript variants in prostate cancer

Niusha Samadaian1, Pouya Salehipour1, Mohsen Ayati2

  • 1Department of Medical Genetics, Tehran University of Medical Sciences, Tehran, 1417613151, Iran.

Insights

This study found that DAB2IP variant 1 and SPRY2 variant 2 are significantly down-regulated in prostate cancer tissues, suggesting their role in prostate tumorigenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Deregulation of signaling pathways is central to cancer development.
  • DAB2IP and SPRY2 are feedback inhibitors of receptor tyrosine kinases in the MAPK pathway.
  • These proteins are implicated in cancer pathophysiology.

Purpose of the Study:

  • To investigate the expression of all known splice variants of DAB2IP and SPRY2 in prostate tissue.
  • To determine the role of DAB2IP and SPRY2 variants in prostate cancer and benign prostatic hyperplasia (BPH).

Main Methods:

  • RNA extraction from fresh prostate tissue samples (prostate cancer, normal, BPH).
  • cDNA synthesis followed by RT-PCR and quantitative Real-time PCR to evaluate transcript variant expression.
  • Correlation analysis with Prostate-Specific Antigen (PSA) levels.

Main Results:

  • Significant down-regulation of DAB2IP transcript variant 1 in cancerous tissues versus normal tissues (P=0.001).
  • Significant down-regulation of SPRY2 transcript variant 2 in cancerous tissues compared to normal and BPH tissues (P=0.008, P=0.025).
  • Negative correlation between DAB2IP.1 and SPRY2.2 expression with PSA levels in prostate cancer.
  • Positive correlation between the down-regulation of DAB2IP.1 and SPRY2.2 mRNA in tumor samples (P=0.002).

Conclusions:

  • This study is the first to highlight the deregulation of DAB2IP and SPRY2 transcript variants in human prostate cancer.
  • Transcript-specific down-regulation of DAB2IP and SPRY2 variants is confirmed and extended.
  • DAB2IP and SPRY2 variants show significant association with prostate tumorigenesis.

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