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  11. The Effect Of Sp/nk1r On Expression And Activity Of Glutaredoxin And Thioredoxin Proteins In Prostate Cancer Cells

The effect of SP/NK1R on expression and activity of glutaredoxin and thioredoxin proteins in prostate cancer cells

Sara Zarei Shandiz1, Reza Assaran Darban2, Hossein Javid3,4

  • 1Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|February 9, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Substance P (SP) and its receptor (NK1R) promote prostate cancer by increasing oxidative stress. Blocking NK1R with aprepitant reversed these effects, suggesting aprepitant as a potential prostate cancer treatment.

Area of Science:

  • Oncology
  • Neuroscience
  • Biochemistry

Background:

  • Substance P (SP) and neurokinin-1 receptor (NK1R) are implicated in prostate cancer progression.
  • Oxidative stress is a known factor in prostate cancer development.
  • The interplay between the SP/NK1R system and redox balance in prostate cancer remains unexplored.

Purpose of the Study:

  • To investigate the impact of the SP/NK1R system on cellular redox status in prostate cancer.
  • To examine the effects of NK1R antagonism with aprepitant on prostate cancer cells.
  • To explore the potential of targeting the SP/NK1R system for prostate cancer therapy.

Main Methods:

  • Utilized prostate cancer cell lines (PC3 and LNCaP).
  • Assessed cell viability using the resazurin assay.
Keywords:
AprepitantGlutaredoxinNeurokinin 1 receptorOxidative stress

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  • Measured intracellular reactive oxygen species (ROS) levels.
  • Quantified the expression and activity of glutaredoxin and thioredoxin via qRT-PCR and commercial kits.

    • Main Results:

    • SP treatment elevated ROS production and reduced glutaredoxin and thioredoxin expression/activity.
    • Aprepitant treatment counteracted the effects of SP, normalizing redox balance.
    • SP/NK1R signaling appears to drive prostate cancer progression via oxidative stress induction.

    Conclusions:

    • The SP/NK1R system contributes to prostate cancer progression by exacerbating oxidative stress.
    • NK1R inhibition with aprepitant modulates cellular redox status, offering a potential therapeutic avenue.
    • Aprepitant shows promise as a candidate for prostate cancer treatment, warranting further investigation.
    Prostate cancer
    Substance P
    Thioredoxin