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CRP and HNF1A collaborate to regulate the progression of laryngeal cancer through the Wnt signaling pathway

  • 0Department of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital, Harbin Medical University, No. 23 Youzheng Street, Nangang District, Harbin City, Heilongjiang Province, 150001, People's Republic of China.
Functional & Integrative Genomics +

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July 27, 2025

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July 27, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

CRP and HNF1A promote laryngeal cancer (LC) progression. Knockdown of these genes inhibits tumor growth, migration, and invasion while enhancing apoptosis, indicating their role in the Wnt signaling pathway and epithelial-mesenchymal transition.

Area Of Science

  • Oncology
  • Molecular Biology
  • Genetics

Background

  • Laryngeal cancer (LC) progression involves complex regulatory mechanisms.
  • Identifying key genes and transcription factors is crucial for understanding LC pathogenesis.

Purpose Of The Study

  • To investigate the regulatory roles of C-reactive protein (CRP) and Hepatocyte Nuclear Factor 1-Alpha (HNF1A) in laryngeal cancer.
  • To elucidate the underlying molecular mechanisms, including the Wnt signaling pathway and epithelial-mesenchymal transition (EMT).

Main Methods

  • Bioinformatics analysis to identify core LC genes and transcription factors.
  • Quantitative Reverse Transcription Polymerase Chain Reaction (QRT-PCR) for gene expression analysis.
  • Cellular assays (CCK-8, flow cytometry, wound-healing, Transwell) for proliferation, apoptosis, migration, and invasion.
  • Dual luciferase assays, ChIP, and EMSA to confirm gene interactions.
  • Western blot and immunohistochemistry for protein expression analysis.
  • In vivo tumorigenesis experiments in nude mice.

Main Results

  • CRP and HNF1A were identified as key genes correlated in LC and were upregulated in human LC tissues.
  • Knockdown of CRP and HNF1A significantly inhibited proliferation, migration, and invasion, while enhancing apoptosis in LC cells.
  • HNF1A knockdown led to downregulation of CRP, β-catenin, Wnt3a, and Vimentin, and upregulation of E-cadherin, suggesting involvement of the Wnt pathway and EMT.
  • In vivo experiments confirmed that CRP knockdown inhibited tumor growth and modulated related protein expressions.

Conclusions

  • CRP and HNF1A act as oncogenes promoting laryngeal cancer progression.
  • These genes exert their effects by activating the Wnt signaling pathway and promoting epithelial-mesenchymal transition.
  • Targeting CRP and HNF1A may represent a potential therapeutic strategy for laryngeal cancer.

Keywords:

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