Over expression of PI3K-AkT reduces apoptosis and increases prostate size in benign prostatic hyperplasia

Karli Sreenivasulu1, Hanumanthappa Nandeesha1, Lalgudi Narayanan Dorairajan2

  • 1Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.

Abstract

Insights

Increased expression of phosphatidylinositol 3-kinase (PI3K)/AKT pathway and BcL-2 is linked to reduced apoptosis and larger prostate size in benign prostatic hyperplasia (BPH). This study investigated these molecular changes in BPH patients.

Area of Science:

  • Urology
  • Molecular Biology
  • Oncology

Background:

  • The phosphatidylinositol 3-kinase (PI3K)/AKT pathway and apoptosis are crucial in prostate cancer.
  • Limited research exists on PI3K/AKT pathway gene expression and apoptotic protein levels in Benign Prostatic Hyperplasia (BPH) and their correlation with prostate size.

Purpose of the Study:

  • To investigate the gene expression of PI3K/AKT pathway components.
  • To analyze the protein expression of apoptotic factors.
  • To determine the association between these molecular alterations and prostate size in BPH patients.

Main Methods:

  • Gene expression of PI3K and AKT was quantified using quantitative PCR (q-PCR).
  • Protein levels of apoptotic markers (BcL-2, caspase-3, caspase-9, BAD, p-BAD) were assessed via western blotting and immunohistochemistry.
  • The study included 27 BPH patients aged 55-75 years.

Main Results:

  • Significant upregulation of PI3K (p85-A), AKT1, and AKT2 gene expression was observed in BPH patients with larger prostates.
  • Protein expression of BcL-2 and caspase-9 was also significantly elevated in larger prostates.
  • These findings suggest a correlation between specific molecular pathways and prostate enlargement.

Conclusions:

  • Overexpression of the PI3K/AKT pathway and BcL-2 is associated with reduced apoptosis.
  • These molecular changes correlate with increased prostate size in Benign Prostatic Hyperplasia.
  • The study highlights potential molecular targets for managing BPH progression.

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