Downregulated Reprimo by LINC00467 participates in the growth and metastasis of gastric cancer

Bioengineered. 2022 May;13(5):11893-11906. doi: 10.1080/21655979.2022.2063662.

Abstract

Gastric cancer (GC) as an aggressive malignancy still causes a global health problem. It has been documented that long noncoding RNAs are involved in GC development. Therefore, this research was designed to explore the role of LINC00467 in the growth and metastasis of GC. The expression of LINC00467 and Reprimo in GC tissues and cells was detected. The binding relationship among LINC00467, DNA methyltransferase 1 (DNMT1) and Reprimo was assessed following. Reprimo promoter methylation was detected by methylation sequencing. GC cell lines overexpressing or knock downing LINC00467 were constructed for pinpointing the effect of LINC00467 on cell functions as well as growth and metastasis of GC cells in vivo. LINC00467 was highly expressed, whereas Reprimo was poorly expressed in GC tissues and cells. Mechanically, LINC00467 promoted the methylation and decreased the expression of Reprimo promoter by recruiting DNMT1 in GC cells. Knockdown of LINC00467 diminished the malignant properties of GC cells. Knockdown of LINC00467 reduced tumorigenesis and metastasis of GC cells in vivo. LINC00467 might exert oncogenic effects in GC via Reprimo downregulation by recruiting DNMT1.

Keywords: DNA methyltransferase; DNMT1; LINC00467; gastric cancer; grow; metastasis; promoter methylation; reprimo; tumor suppressor gene.

MeSH terms

  • Cell Cycle Proteins*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • DNA Methylation / genetics
  • Down-Regulation / genetics
  • Gene Expression Regulation, Neoplastic
  • Glycoproteins*
  • Humans
  • Promoter Regions, Genetic
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism
  • Stomach Neoplasms* / pathology

Substances

  • Cell Cycle Proteins
  • Glycoproteins
  • RNA, Long Noncoding
  • RPRM protein, human

Grants and funding

The author(s) reported there is no funding associated with the work featured in this article.