Long non-coding RNA LGALS8-AS1 facilitates PLAGL2-mediated malignant phenotypes in gastric cancer

Gang Wang1,2, Kuan Shen1, Jian Xiao1

  • 1Department of General Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.

Abstract

Insights

This study identifies long non-coding RNA LGALS8-AS1 as a promoter of gastric cancer (GC) progression. Upregulated LGALS8-AS1 facilitates GC cell proliferation and metastasis by sponging miR-138-5p and increasing PLAGL2 expression, suggesting it as a potential GC therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Gastric cancer (GC) research has advanced, but many long non-coding RNAs (lncRNAs) roles remain unexplored.
  • Identifying novel lncRNAs is crucial for understanding GC tumorigenesis and developing new therapies.

Purpose of the Study:

  • To identify and characterize novel gastric cancer-related lncRNAs.
  • To elucidate the functional role and molecular mechanism of LGALS8-AS1 in GC progression.

Main Methods:

  • Utilized The Cancer Genome Atlas (TCGA) database and bioinformatics survival analysis to identify LGALS8-AS1.
  • Employed quantitative real-time polymerase chain reaction (qRT-PCR) for expression analysis.
  • Conducted in vitro and in vivo experiments to assess the functional role of LGALS8-AS1 and its downstream targets (miR-138-5p, PLAGL2).

Main Results:

  • LGALS8-AS1 was significantly upregulated in GC and associated with poor prognosis, higher lymph node metastasis, and larger tumor size.
  • LGALS8-AS1 promoted GC cell proliferation, migration, and metastasis both in vitro and in vivo.
  • LGALS8-AS1 acts as a molecular sponge for miR-138-5p, leading to increased PLAGL2 expression and subsequent promotion of GC progression.

Conclusions:

  • The LGALS8-AS1/miR-138-5p/PLAGL2 axis plays a significant role in promoting gastric cancer.
  • LGALS8-AS1 represents a potential diagnostic and therapeutic target for gastric cancer.
  • Findings enhance understanding of GC tumorigenesis and development mechanisms.

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