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Updated: Aug 8, 2026

RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
09:36

RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA

Published on: April 10, 2018

Long non-coding RNA MEG3 induces cell apoptosis in esophageal cancer through endoplasmic reticulum stress

Zhen-Lun Huang1, Rui-Pei Chen1, Xiao-Tao Zhou1

  • 1Department of Gastroenterology, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong 515041, P.R. China.

Oncology Reports
|April 14, 2017
PubMed

Insights

Long non-coding RNA MEG3 is downregulated in esophageal squamous cell carcinoma (ESCC). Overexpressing MEG3 inhibits ESCC cell growth and induces apoptosis, likely by activating endoplasmic reticulum stress pathways.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) regulate critical cellular functions.
  • The role of lncRNA MEG3 in esophageal squamous cell carcinoma (ESCC) is largely unknown.
  • MEG3 downregulation is observed in various cancers.

Purpose of the Study:

  • To quantify MEG3 expression in ESCC tissues.
  • To elucidate the functional role of MEG3 in ESCC.
  • To investigate the involvement of endoplasmic reticulum (ER) stress in MEG3's mechanism.

Main Methods:

  • Quantitative reverse transcription PCR (qRT-PCR) for MEG3 expression analysis.
  • Transfection of EC109 cells with MEG3-expressing plasmids.
  • Cell proliferation assays (CCK-8) and apoptosis assays (Annexin V/PI).
  • Western blot analysis for ER stress-related proteins.

Main Results:

  • MEG3 expression was significantly reduced in ESCC tissues compared to adjacent normal tissues.
  • MEG3 overexpression in EC109 cells suppressed cell proliferation and promoted apoptosis.
  • MEG3 upregulation led to increased expression of ER stress markers (GRP78, IRE1, PERK, ATF6, CHOP) and cleaved-caspase-3.

Conclusions:

  • This study demonstrates MEG3 downregulation in ESCC.
  • MEG3 inhibits ESCC cell growth and induces apoptosis in vitro.
  • MEG3 likely exerts its tumor-suppressive effects through the activation of the ER stress pathway.

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