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Suppression of Long Noncoding RNA SNHG1 Inhibits the Development of Hypopharyngeal Squamous Cell Carcinoma via

Qian Chen1, Xiao He1, Bin Li1

  • 1Department of Otolaryngology, The First Affiliated Hospital of Zhejiang Traditional Chinese Medical University, Hangzhou 310006, China.

Evidence-Based Complementary and Alternative Medicine : Ecam
|July 15, 2022
PubMed
Abstract

Insights

Long noncoding RNA SNHG1 promotes hypopharyngeal squamous cell carcinoma (HSCC) progression by upregulating PARP6. Silencing SNHG1 inhibits HSCC, suggesting SNHG1/PARP6 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • RNA Biology

Background:

  • Hypopharyngeal squamous cell carcinoma (HSCC) is a challenging malignancy.
  • Understanding the molecular mechanisms driving HSCC is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role and molecular mechanism of long noncoding RNA Small Nucleolar RNA Host Gene 1 (SNHG1) in HSCC development.
  • To explore the SNHG1/PARP6 axis in HSCC pathogenesis.

Main Methods:

  • Utilized the human HSCC cell line FaDu for in vitro experiments.
  • Assessed cell viability, apoptosis, migration, and invasion using CCK-8, flow cytometry, and Transwell assays.
  • Determined protein expression of key molecules including PARP6, XRCC6, β-catenin, E-cadherin, and N-cadherin via Western blotting.
  • Investigated the SNHG1-PARP6 regulatory relationship and in vivo tumorigenicity.

Main Results:

  • SNHG1 suppression reduced HSCC cell viability, migration, and invasion while promoting apoptosis.
  • PARP6 was identified as a target of SNHG1 and was upregulated by SNHG1 knockdown.
  • The SNHG1/PARP6 axis significantly inhibited HSCC cell proliferation, migration, invasion, and in vivo tumorigenicity.
  • SNHG1 suppression or PARP6 overexpression altered the expression of EMT markers, increasing E-cadherin and decreasing N-cadherin, β-catenin, and XRCC6.

Conclusions:

  • SNHG1 silencing inhibits HSCC progression by upregulating PARP6.
  • The XRCC6/β-catenin/EMT pathway may mediate the downstream effects of the SNHG1/PARP6 axis in HSCC.
  • The SNHG1/PARP6 axis represents a promising therapeutic target for HSCC treatment.

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