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Silencing of Long Non-Coding RNA Colon Cancer-Associated Transcript 2 Inhibits the Growth and Metastasis of Gastric

Sen Lin1, Hongbo Wang1, Wenjuan Yang2

  • 1Department of Gastroenterology, The Second Hospital of Shandong University, Jinan City, Shangdong 250033, People's Republic of China.

Oncotargets and Therapy
|February 6, 2020
PubMed
Abstract

Insights

Silencing colon cancer-associated transcript 2 (CCAT2) inhibits gastric cancer (GC) progression by reducing proliferation, migration, and invasion, while enhancing apoptosis and autophagy through the mammalian target of rapamycin (mTOR) signaling pathway.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Gene Regulation

Background:

  • Gastric cancer (GC) remains a significant global health challenge with complex molecular underpinnings.
  • The role of long non-coding RNAs, such as colon cancer-associated transcript 2 (CCAT2), in GC pathogenesis is increasingly recognized.
  • Understanding the regulatory pathways, including mammalian target of rapamycin (mTOR) signaling, is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the specific function of CCAT2 in gastric cancer (GC) development and progression.
  • To elucidate the potential regulatory mechanism of CCAT2 involving the mammalian target of rapamycin (mTOR) signaling pathway.

Main Methods:

  • CCAT2 expression was quantified in GC tissues and cell lines using quantitative real-time PCR (qRT-PCR).
  • CCAT2 was silenced using siRNA in HGC-27 and SGC-7901 cells; mTOR signaling was activated using Leucine (Leu) in HGC-27 cells.
  • Cell proliferation, cell cycle, apoptosis, migration, invasion, and autophagy were assessed using various assays, alongside Western blot analysis for key protein markers.

Main Results:

  • CCAT2 was significantly upregulated in GC tissues and cells, correlating with advanced tumor stage, lymphatic metastasis, and poorer survival rates.
  • Silencing CCAT2 inhibited GC cell proliferation, colony formation, migration, and invasion, while inducing G0/G1 cell cycle arrest, apoptosis, and autophagy.
  • CCAT2 knockdown led to altered expression of proliferation, invasion, apoptosis, autophagy, and mTOR signaling markers, and reversed the tumor-promoting effects of mTOR activation.

Conclusions:

  • CCAT2 plays a critical role in promoting gastric cancer progression.
  • Silencing CCAT2 effectively inhibits GC cell proliferation, migration, and invasion, while promoting apoptosis and autophagy.
  • These anti-tumor effects are mediated, at least in part, by the inhibition of the mTOR signaling pathway.
Keywords:
apoptosisautophagycolon cancer-associated transcript 2gastric cancermammalian target of rapamycin

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