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Silencing lncRNA AGAP2-AS1 Upregulates miR-195-5p to Repress Migration and Invasion of EC Cells via the Decrease of

Sining Shen1, Ke Li2, Ying Liu2

  • 1Department of Thoracic Surgery, Affiliated Cancer Hospital of Zhengzhou University (Henan Cancer Hospital), Zhengzhou 450008, P.R. China.

Molecular Therapy. Nucleic Acids
|March 22, 2020
PubMed

Insights

Targeting AGAP2-AS1, a long non-coding RNA, can suppress esophageal cancer (EC) progression. This involves upregulating miR-195-5p and downregulating FOSL1, offering a potential new therapeutic strategy for EC.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs) interactions are crucial in cancer development.
  • Esophageal cancer (EC) progression is influenced by complex molecular pathways.
  • Understanding the specific roles of lncRNA/miRNA/mRNA axes is vital for targeted therapies.

Purpose of the Study:

  • To investigate the role of the AGAP2-AS1/miR-195-5p/FOSL1 axis in esophageal cancer (EC) progression.
  • To elucidate the molecular mechanisms underlying EC development involving these key molecules.
  • To evaluate the therapeutic potential of targeting this axis in EC.

Main Methods:

  • Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) to determine expression levels of AGAP2-AS1, miR-195-5p, and FOSL1.
  • In vitro experiments including ectopic expression, knockdown, and reporter assays to study cellular processes.
  • In vivo studies to assess the effect of AGAP2-AS1 silencing on tumor growth.

Main Results:

  • AGAP2-AS1 and FOSL1 were upregulated, while miR-195-5p was downregulated in EC tissues and cell lines.
  • AGAP2-AS1 knockdown or miR-195-5p overexpression inhibited EC cell proliferation, migration, and invasion, and promoted apoptosis.
  • miR-195-5p directly targets FOSL1, and AGAP2-AS1 upregulates FOSL1 by sponging miR-195-5p.

Conclusions:

  • AGAP2-AS1 promotes EC development by upregulating FOSL1 via sponging miR-195-5p.
  • Silencing AGAP2-AS1 restrains EC progression both in vitro and in vivo.
  • Targeting AGAP2-AS1 represents a promising therapeutic strategy for esophageal cancer.
Keywords:
FOSL1apoptosisesophageal cancerinvasionlong non-coding AGAP2-AS1microRNA-195-5pmigrationproliferation

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