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JAK/STAT Dysregulation With SOCS1 Overexpression in Acquired Cholesteatoma-Adjacent Mucosa

Johanna Westerberg1, Ellen Tideholm2, Krzysztof Piersiala2,3

  • 1Department of Biomedical and Clinical Sciences, Division of Sensory Organs and Communication, Linköping University, Region Östergötland, Sweden.

Otology & Neurotology : Official Publication of the American Otological Society, American Neurotology Society [And] European Academy of Otology and Neurotology
|November 17, 2020
PubMed
Abstract

Insights

This study found that the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is altered in cholesteatoma. Specifically, suppressor of cytokine signaling-1 (SOCS1) was upregulated and STAT5B was downregulated in affected tissues.

Area of Science:

  • Otolaryngology
  • Molecular Biology
  • Immunology

Background:

  • Surgery is the primary treatment for cholesteatoma, but recurrence rates remain high.
  • Nonsurgical treatment alternatives targeting molecular pathways are needed.
  • The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is a potential therapeutic target.

Purpose of the Study:

  • To investigate the JAK/STAT pathway in middle ear mucosa of patients with acquired cholesteatoma.
  • To compare the expression of key JAK/STAT pathway components in cholesteatoma tissue versus healthy controls.

Main Methods:

  • A case-control study was conducted involving 26 patients with acquired cholesteatoma and 27 healthy controls.
  • Quantitative polymerase chain reaction (qPCR) was used to measure the expression of Interleukin-7 receptor alpha, JAK1, JAK2, JAK3, STAT5A, STAT5B, and SOCS1.
  • Additional markers including cyclin D2, TGF-β1, TSLP, CD3, and CD19 were evaluated.

Main Results:

  • Suppressor of cytokine signaling-1 (SOCS1) was significantly upregulated in cholesteatoma-adjacent mucosa compared to healthy controls (p=0.0003).
  • STAT5B was significantly downregulated in cholesteatoma-adjacent mucosa compared to healthy controls (p=0.0006).
  • No significant differences in JAK1, JAK2, JAK3, or STAT5A expression were observed between the groups.

Conclusions:

  • This study is the first to report JAK/STAT pathway dysregulation in cholesteatoma-adjacent mucosa.
  • Key components of the JAK/STAT pathway, SOCS1 and STAT5B, are significantly altered in cholesteatoma.
  • These findings suggest the JAK/STAT pathway as a potential target for novel nonsurgical cholesteatoma treatments.

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