Long noncoding RNA DINO (damage induced noncoding) represses the development of gastric cancer by modulating p21 and

Qinqiang Liu1, Yan Xiao2, Peng Cai1

  • 1Department of General Surgery, Xuzhou Hospital of Traditional Chinese medicine, Xuzhou, Jiangsu, China.

Insights

Long non-coding RNA damage induced noncoding (DINO) is downregulated in gastric cancer (GC). Restoring DINO suppresses GC cell proliferation and promotes apoptosis, suggesting its tumor-inhibitory role.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are implicated in various diseases, including gastric cancer (GC).
  • The specific role of lncRNA damage induced noncoding (DINO) in GC progression has been underexplored.
  • lncRNAs function as critical regulators of gene expression.

Purpose of the Study:

  • To investigate the biological function and mechanism of lncRNA DINO in gastric cancer.
  • To determine the expression levels of DINO in GC tissues and cell lines.
  • To elucidate the effect of DINO modulation on GC cell behavior.

Main Methods:

  • Quantitative analysis of DINO expression in GC tissues.
  • Overexpression and knockdown of DINO in GC cell lines (BGC-823, MGC-803) using lentiviral vectors.
  • Assessment of cell proliferation, apoptosis, and cell cycle progression.
  • Western blot analysis to detect protein expression levels of p21 and Bax.

Main Results:

  • DINO expression was significantly downregulated in GC tissues compared to normal tissues.
  • Overexpression of DINO suppressed GC cell proliferation and induced apoptosis.
  • Silencing DINO enhanced GC cell proliferation and inhibited apoptosis.
  • DINO overexpression led to cell cycle arrest and increased expression of p21 and Bax.
  • DINO inhibition decreased p21 and Bax protein levels.

Conclusions:

  • DINO acts as a tumor suppressor in gastric cancer.
  • DINO exerts its inhibitory effects by promoting apoptosis and cell cycle arrest.
  • The tumor-suppressive function of DINO may be mediated through the modulation of p21 and Bax expression in GC.

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