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ZNF703 is an important player in head and neck cancer

Ceren Orhan1, Burak Bakır1, Nejat Dalay1

  • 1Department of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey.

Clinical Otolaryngology : Official Journal of ENT-UK ; Official Journal of Netherlands Society for Oto-Rhino-Laryngology & Cervico-Facial Surgery
|October 2, 2019
PubMed
Abstract

Insights

Head and neck squamous cell carcinoma (HNSCC) shows increased Zinc finger protein 703 (ZNF703) expression, linked to gene amplification. This over-expression may activate the PI3K/Akt pathway, offering new therapeutic targets for HNSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Head and neck squamous cell carcinoma (HNSCC) presents significant treatment challenges with limited survival improvements.
  • Understanding the molecular underpinnings of HNSCC is crucial for developing effective therapies.
  • Zinc finger protein 703 (ZNF703) is an oncogenic transcription factor implicated in various cancers due to chromosome 8p12 amplification.

Purpose of the Study:

  • To investigate the expression patterns of ZNF703 in HNSCC.
  • To analyze the association between ZNF703 expression, CCND1 expression, and Akt phosphorylation in HNSCC.
  • To explore the molecular mechanisms driving HNSCC development and progression.

Main Methods:

  • Prospective study involving 105 HNSCC patients.
  • Analysis of 50 HNSCC tumor and non-cancerous tissue samples using qRT-PCR and Western blotting.
  • Correlation of ZNF703 expression with clinicopathological features, copy number variation, and survival data.

Main Results:

  • ZNF703 gene expression was elevated in 22.9% of HNSCC tumor tissues compared to normal counterparts.
  • ZNF703 over-expression was found to be associated with copy number variation.
  • Preliminary findings suggest a link between ZNF703 over-expression and the activation of the PI3K/Akt signaling pathway.

Conclusions:

  • ZNF703 over-expression is linked to copy number variations in HNSCC.
  • The over-expression of ZNF703 may contribute to HNSCC pathogenesis by activating the PI3K/Akt signaling pathway.
  • Further research into ZNF703's role could reveal novel therapeutic strategies for HNSCC.
Keywords:
Akt phosphorylationCCND1HNSCCPI3K/Akt signallingZNF703copy number variationqRT-PCR

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