Knockdown of Long Noncoding RNA Small Nucleolar RNA Host Gene 12 Inhibits Cell Growth and Induces Apoptosis by

Xiaoyan Wang1, Guanbin Qi1, Juanjuan Zhang1

  • 1Department of Pneumology, Huaihe Hospital of Henan University , Kaifeng, China .

DNA and Cell Biology
|September 6, 2017
PubMed

Insights

Small nucleolar RNA host gene 12 (SNHG12) is overexpressed in nonsmall cell lung cancer (NSCLC). Reducing SNHG12 inhibits NSCLC growth and promotes apoptosis by increasing miR-138 levels.

Area of Science:

  • Molecular Biology
  • Oncology
  • RNA Biology

Background:

  • Small nucleolar RNA host gene 12 (SNHG12) is a long noncoding RNA implicated as an oncogene in various cancers.
  • The specific role of SNHG12 in nonsmall cell lung cancer (NSCLC) pathogenesis and its molecular targets remain underexplored.

Purpose of the Study:

  • To investigate the role of SNHG12 in NSCLC development.
  • To elucidate the regulatory relationship between SNHG12 and miR-138 in NSCLC cells.

Main Methods:

  • Quantitative real-time PCR to assess SNHG12 and miR-138 expression levels in NSCLC cells and normal lung epithelial cells.
  • Western blotting to measure caspase-3 activity.
  • Cell proliferation assays, colony formation assays, and apoptosis assays.
  • In vivo studies using a NSCLC mouse xenograft model.

Main Results:

  • SNHG12 was significantly upregulated, and miR-138 was downregulated in NSCLC cells compared to normal controls.
  • SNHG12 directly binds to miR-138, negatively regulating its expression.
  • Knockdown of SNHG12 suppressed NSCLC cell proliferation, colony formation, and induced apoptosis, evidenced by increased caspase-3 activity.
  • Restoration of miR-138 partially reversed the effects of SNHG12 knockdown.
  • In vivo, SNHG12 knockdown significantly reduced tumor volume and weight in the NSCLC mouse model.

Conclusions:

  • SNHG12 acts as an oncogene in NSCLC by downregulating miR-138.
  • Targeting SNHG12 represents a potential therapeutic strategy for NSCLC by inhibiting tumor growth and inducing apoptosis.

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