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Interactions Between Signaling Pathways

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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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STAT3 Post-Translational Modifications Drive Cellular Signaling Pathways in Prostate Cancer Cells.

Rossana Cocchiola1, Elisabetta Rubini2, Fabio Altieri3

  • 1Department of Biochemical Sciences "A. Rossi Fanelli" and Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University, P.le A. Moro 5, 00185 Rome, Italy. rossana.cocchiola@uniroma1.it.

International Journal of Molecular Sciences
|April 25, 2019
PubMed
Summary
This summary is machine-generated.

This study reveals how specific modifications to STAT3 (Signal Transducer and Activator of Transcription 3) proteins change in response to different cellular conditions, offering new therapeutic targets for prostate cancer (PCa). Understanding these STAT3 post-translational modifications (PTMs) is key for developing effective PCa treatments.

Keywords:
STAT3post translational modificationprostate cancertransduction signaling

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Signal Transducer and Activator of Transcription 3 (STAT3) is an oncoprotein frequently overexpressed in various cancers, including prostate cancer (PCa).
  • STAT3 activity is regulated by post-translational modifications (PTMs), which can differ based on cellular conditions like inflammation and oxidative stress.
  • Prostate cancer progression involves distinct microenvironments, with inflammation prevalent in early stages and oxidative stress in advanced disease.

Purpose of the Study:

  • To investigate the relationship between stimulus-specific STAT3 PTMs and STAT3-mediated transcriptional programs in prostate cancer.
  • To identify potential new pharmacological targets for PCa treatment by understanding how STAT3 PTMs are modulated by different cellular stresses.

Main Methods:

  • Experiments were conducted on LNCaP (less aggressive) and DU-145 (more aggressive) prostate cancer cell lines.
  • Cellular models simulated inflammatory conditions (using IL-6) and oxidative stress (using tert-butyl hydroperoxyde, tBHP).
  • Analysis included identifying specific STAT3 PTMs (phosphorylation, acetylation, and glutamylation) and their interaction with proteins like P300 and APE1/Ref-1.

Main Results:

  • Phosphorylated STAT3 at tyrosine 705 (pY705-STAT3) was identified as a common signaling component across all tested conditions.
  • Specific PTMs were observed in response to stimuli: acetylation at lysine 685 (acK685-STAT3) with IL-6, and glutamylation (glutC328/542-STAT3) and phosphorylation at serine 727 (pS727-STAT3) with tBHP.
  • An interplay between STAT3 PTMs and interacting proteins (P300, APE1/Ref-1) was confirmed, influencing STAT3-target gene expression.

Conclusions:

  • STAT3 PTMs exhibit stimulus-specificity, correlating with distinct STAT3-mediated transcriptional outputs in prostate cancer cells.
  • These findings highlight STAT3 and its diverse PTMs as critical drivers in prostate cancer progression.
  • The stimulus-response patterns of STAT3 PTMs offer promising avenues for targeted therapeutic strategies in PCa.