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p53-Induced LINC00893 Regulates RBFOX2 Stability to Suppress Gastric Cancer Progression

Xinde Ou1,2, Xingyu Zhou1,2, Jin Li1,2,3

  • 1Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Frontiers in Cell and Developmental Biology
|February 7, 2022
PubMed

Insights

Long intergenic non-protein coding RNA 00893 (LINC00893) acts as a tumor suppressor in gastric cancer (GC). It inhibits GC cell proliferation and metastasis by regulating epithelial-mesenchymal transition (EMT) via RBFOX2, offering a new target for GC treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) play roles in cancer.
  • The function of LINC00893 in gastric cancer (GC) is largely unknown.

Purpose of the Study:

  • To investigate the biological functions and molecular mechanisms of LINC00893 in GC.

Main Methods:

  • Quantitative analysis of LINC00893 expression in GC tissues and cells.
  • Functional assays (proliferation, migration, invasion) upon LINC00893 manipulation.
  • Mechanism studies involving RNA binding fox-1 homolog 2 (RBFOX2) and epithelial-mesenchymal transition (EMT) markers.
  • Investigation of p53 regulation on LINC00893.

Main Results:

  • LINC00893 expression was decreased in GC tissues and correlated with poor prognosis.
  • Overexpression of LINC00893 suppressed GC cell proliferation, migration, and invasion.
  • LINC00893 binds to RBFOX2, promoting its degradation and inhibiting EMT.
  • p53 indirectly regulates LINC00893 expression.

Conclusions:

  • LINC00893 acts as a tumor-suppressive lncRNA in GC, induced by p53.
  • LINC00893 inhibits GC progression by suppressing EMT through RBFOX2 degradation.
  • LINC00893 represents a potential therapeutic target for GC.
Keywords:
LINC00893RBFOX2epithelial-mesenchymal transitiongastric cancerp53

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