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Related Experiment Video

Updated: Jun 29, 2025

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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LncRNA SNHG26 promotes gastric cancer progression and metastasis by inducing c-Myc protein translation and an energy

Zhen-Hua Wu1,2, Yi-Xuan Wang1,2, Jun-Jiao Song2,3

  • 1Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.

Cell Death & Disease
|March 30, 2024
PubMed
Summary
This summary is machine-generated.

Small nucleolar RNA host gene 26 (SNHG26) promotes gastric cancer (GC) metastasis by enhancing cell proliferation and epithelial-mesenchymal transition. Targeting this pathway offers potential therapeutic strategies for GC treatment.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cancer metastasis presents a significant challenge in effective cancer treatment.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in regulating cancer metastasis, but their specific involvement in gastric cancer (GC) requires further elucidation.

Purpose of the Study:

  • To identify novel metastasis-associated lncRNAs in gastric cancer (GC).
  • To investigate the functional role and underlying mechanism of SNHG26 in GC progression.
  • To explore the therapeutic potential of targeting the SNHG26 pathway in GC.

Main Methods:

  • RNA sequencing (RNA-seq) on metastasis-inclined GC tissues.
  • In vitro and in vivo functional experiments assessing cell proliferation and epithelial-mesenchymal transition (EMT).
  • Mechanistic studies involving nucleolin (NCL) interaction, c-Myc translation modulation, and hexokinase 2 (HK2)-mediated energy metabolism analysis.

Main Results:

  • Upregulated SNHG26 expression was identified in GC tissues and correlated with poor patient prognosis.
  • SNHG26 significantly promoted GC cell proliferation and EMT both in vitro and in vivo.
  • SNHG26 interacts with NCL to enhance c-Myc translation, subsequently boosting HK2-driven energy metabolism, creating a positive feedback loop that fuels GC malignancy.

Conclusions:

  • SNHG26 is a key driver of GC metastasis and progression.
  • The SNHG26/NCL/c-Myc/HK2 axis represents a critical regulatory pathway in GC.
  • Inhibiting this metabolic and translational feedback loop with specific inhibitors shows promise for developing novel GC therapeutics.