LncRNA EPIC1 promotes proliferation and inhibits apoptosis of gallbladder cancer cells by interacting with LET

Ann Hepatol. 2021 Dec:26:100563. doi: 10.1016/j.aohep.2021.100563. Epub 2021 Oct 13.

Abstract

Introduction and objectives: Long non-coding RNA (lncRNA) EPIC1 (epigenetically-induced lncRNA1) is likely involved in human cancer by promoting cell cycle progression. Our study was carried out to investigate the involvement of EPIC1 in gallbladder cancer (GBC).

Methods: Expression levels of EPIC1 in two types of tissues (GBC and paracancerous) and plasma were measured by performing qPCR. GBC-SD and SGC-996 cells were transfected with low expression in tumor (LET) and EPIC1 expression vectors.

Results: The present study found that EPIC1 was upregulated in tumor tissues than in paracancerous tissues of GBC patients, and plasma levels of EPIC1 were significantly correlated with levels of EPIC1 in tumor tissues. LncRNA LET was downregulated in tumor tissues than in paracancerous tissues and was inversely correlated with EPIC1 in both tumor tissues and paracancerous tissues. Overexpression of EPIC1 led to downregulated LET, and LET overexpression also mediated the downregulation of EPIC1. EPIC1 led to accelerated GBC cell proliferation and inhibited apoptosis. Overexpression of LET played opposites roles. In addition, LET overexpression attenuated the effects of EPIC1 overexpression on cancer cell proliferation and apoptosis.

Conclusions: LncRNA EPIC1 promoted proliferation and inhibited apoptosis of GBC cells by interacting with LET.

Keywords: EPIC1; Gallbladder cancer; LET; apoptosis; proliferation.

MeSH terms

  • Aged
  • Apoptosis / genetics*
  • Cell Proliferation / genetics
  • Down-Regulation*
  • Female
  • Follow-Up Studies
  • Gallbladder / metabolism
  • Gallbladder / pathology*
  • Gallbladder Neoplasms / genetics*
  • Gallbladder Neoplasms / metabolism
  • Gallbladder Neoplasms / pathology
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Middle Aged
  • RNA, Long Noncoding / genetics*
  • Retrospective Studies
  • Tumor Cells, Cultured
  • Up-Regulation*

Substances

  • RNA, Long Noncoding