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Down-regulation of long non-coding RNA DUXAP8 suppresses proliferation, metastasis and EMT by modulating miR-498

X Ji1, R Tao, L-Y Sun

  • 1Department of Respiratory and Critical Care Medicine, Lin Yi People's Hospital, Lin Yi, Shandong, China. ycknpi@163.com.

European Review for Medical and Pharmacological Sciences
|April 10, 2020
PubMed
Abstract

Insights

Long non-coding RNA DUXAP8 promotes non-small-cell lung cancer (NSCLC) progression by inhibiting miR-498 and activating the TRIM44-AKT/mTOR pathway. Knockdown of DUXAP8 suppressed tumor growth and metastasis in vivo.

Area of Science:

  • Oncology
  • Molecular Biology
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs) play crucial roles in cancer development.
  • The specific role of DUXAP8 in non-small-cell lung cancer (NSCLC) requires further elucidation.

Purpose of the Study:

  • To investigate the biological function and molecular mechanism of DUXAP8 in NSCLC.
  • To explore the regulatory network involving DUXAP8, miR-498, and TRIM44 in NSCLC.

Main Methods:

  • Quantitative Real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Cell proliferation, migration, and invasion assays (MTT, transwell).
  • Western blot for protein expression, luciferase reporter and RNA pull-down assays for target validation, and in vivo tumor xenograft models.

Main Results:

  • DUXAP8 and TRIM44 were upregulated, while miR-498 was downregulated in NSCLC.
  • DUXAP8 knockdown inhibited NSCLC cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and AKT/mTOR phosphorylation.
  • DUXAP8 regulates TRIM44 via miR-498, and DUXAP8 knockdown reduced tumor growth and metastasis in vivo.

Conclusions:

  • LncRNA DUXAP8 promotes NSCLC cell proliferation, metastasis, and EMT.
  • DUXAP8 exerts its function by inhibiting miR-498, leading to the activation of the TRIM44-mediated AKT/mTOR pathway.
  • DUXAP8 is a potential therapeutic target for NSCLC.

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