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The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal

Weizhen Huang1, Yunming Tian2, Shaoting Dong3

  • 1Department of Medical Oncology, Huizhou Municipal Central Hospital of Guangdong Province, Huizhou, Guangdong 516000, P.R. China.

Oncology Reports
|July 22, 2017
PubMed

Insights

Small nucleolar RNA host gene 3 (SNHG3) promotes colorectal cancer (CRC) progression. Upregulated SNHG3 enhances CRC cell proliferation by sponging miR-182-5p, leading to increased c-Myc expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrantly expressed long non-coding RNAs (lncRNAs) are implicated in colorectal cancer (CRC) development.
  • The specific role of Small nucleolar RNA host gene 3 (SNHG3) in CRC remains largely unelucidated.

Purpose of the Study:

  • To investigate the clinical significance and biological function of SNHG3 in colorectal cancer.
  • To elucidate the molecular mechanism underlying SNHG3's role in CRC progression.

Main Methods:

  • Analysis of TCGA database for SNHG3 expression and patient prognosis.
  • In vitro gain-of-function and loss-of-function assays in CRC cells.
  • Gene Set Enrichment Analysis (GSEA) to identify associated pathways.
  • Mechanistic studies involving RNA immunoprecipitation and luciferase reporter assays to confirm the ceRNA mechanism.

Main Results:

  • SNHG3 expression is significantly upregulated in CRC tissues and correlates with poor patient prognosis.
  • SNHG3 overexpression promotes CRC cell proliferation, while SNHG3 inhibition suppresses it.
  • High SNHG3 expression is positively associated with c-Myc and its target genes.
  • SNHG3 acts as a competing endogenous RNA (ceRNA) by sponging miR-182-5p, thereby upregulating c-Myc expression.

Conclusions:

  • SNHG3 promotes colorectal cancer progression.
  • The SNHG3/miR-182-5p/c-Myc axis represents a potential therapeutic target for CRC.

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