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LncRNA FENDRR suppresses the progression of NSCLC via regulating miR-761/TIMP2 axis

Guijun Zhang1, Qinqin Wang2, Xiaojuan Zhang3

  • 1Ultrasonic Department, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266555, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|September 24, 2019
PubMed

Insights

Long noncoding RNA FENDRR suppresses non-small cell lung cancer (NSCLC) progression by inhibiting miR-761 and regulating TIMP2 expression. This finding offers potential therapeutic targets for NSCLC treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
  • Long noncoding RNAs (lncRNAs) play crucial roles in cancer development and progression.
  • The specific role of lncRNA FENDRR in NSCLC remains largely unexplored.

Purpose of the Study:

  • To investigate the functional role of lncRNA FENDRR in human non-small cell lung cancer (NSCLC).
  • To elucidate the underlying molecular mechanisms of FENDRR in regulating NSCLC cell aggressiveness and tumor growth.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to analyze FENDRR expression levels in NSCLC tissues and cells.
  • In vitro assays including MTT, colony formation, wound closure, and Transwell invasion assays to assess cell proliferation, viability, migration, and invasion.
  • In vivo studies using a xenograft mouse model to evaluate FENDRR's impact on tumor growth.
  • Bioinformatics analysis, luciferase reporter gene assays, and cotransfection experiments to identify molecular interactions and regulatory pathways.

Main Results:

  • FENDRR expression was significantly altered in NSCLC cells and tissues.
  • FENDRR suppressed NSCLC cell proliferation, colony formation, migration, and invasion.
  • FENDRR inhibited tumor growth in vivo.
  • FENDRR directly interacted with miR-761, and this interaction was crucial for FENDRR's tumor-suppressive effects.
  • Tissue inhibitor of metalloproteinase 2 (TIMP2) was identified as a downstream target of miR-761, and its expression was positively regulated by FENDRR.
  • Downregulation of TIMP2 rescued the inhibitory effects of FENDRR on NSCLC cell aggressiveness.

Conclusions:

  • lncRNA FENDRR acts as a tumor suppressor in NSCLC.
  • FENDRR suppresses NSCLC progression by sponging miR-761 and subsequently regulating the expression of its target gene, TIMP2.
  • The FENDRR/miR-761/TIMP2 axis represents a potential therapeutic target for NSCLC treatment.
Keywords:
FENDRRInvasionMiR-761MigrationNSCLCTIMP2

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