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p38 Expression and Modulation of STAT3 Signaling in Oral Cancer.

I Gkouveris1, N Nikitakis2, A Sklavounou2

  • 1Department of Oral Pathology and Medicine, Dental School, National and Kapodistrian University of Athens, 2 Thivon Str. Goudi, 11527, Athens, Greece. igkouver@gmail.com.

Pathology Oncology Research : POR
|March 23, 2018
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Summary

p38 protein is highly expressed in oral squamous cell carcinoma (OSCC) but does not influence the STAT3 pathway. However, p38 inhibition mildly reduced cell growth and viability, suggesting its role in head and neck squamous cell carcinoma (HNSCC).

Keywords:
Oral cancerSTAT3Tumor gradep38

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • p38 protein, part of the Mitogen-activated protein kinases family, regulates fundamental cellular processes.
  • Persistent STAT3 activation is linked to proliferation, differentiation, and apoptosis in oral squamous cell carcinoma (OSCC).

Purpose of the Study:

  • To investigate the effects of p38 modulation on STAT3 signaling and cellular activities in OSCC.
  • To explore the correlation between p38 expression and tumor differentiation in OSCC.

Main Methods:

  • Immunohistochemistry for phospho-p38 in 60 OSCC specimens.
  • Western blot analysis for STAT3, p38, and cyclin D1 in OSCC cell lines.
  • Pharmacological inhibition of p38 using SB203580, followed by assessment of cell proliferation and viability.

Main Results:

  • High phospho-p38 immunoexpression was observed in most OSCC tumors, but without correlation to tumor differentiation.
  • p38 inhibition did not significantly alter STAT3 phosphorylation or cyclin D1 levels.
  • p38 inhibition led to a mild, dose-dependent decrease in cell proliferation and viability in OSCC cell lines.

Conclusions:

  • p38 is highly expressed in OSCC but does not appear to mediate the oncogenic STAT3 pathway.
  • p38 modulation impacts cell proliferation and viability, suggesting a regulatory role in head and neck squamous cell carcinoma (HNSCC).
  • Further understanding of p38 signaling complexity is crucial for developing novel cancer therapies.