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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization

Published on: June 7, 2016

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lncRNA SNHG3 promotes breast cancer progression by acting as a miR‑326 sponge

Haipeng Zhang1, Na Wei2, Wei Zhang3

  • 1Department of Gynecology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Oncology Reports
|September 18, 2020
PubMed

Insights

The long noncoding RNA small nucleolar RNA host gene 3 (SNHG3) is upregulated in breast cancer, promoting tumor growth and metastasis by acting as a competing endogenous RNA (ceRNA) for miR-326. Inhibiting SNHG3 suppressed cancer progression, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
  • The specific function and mechanism of small nucleolar RNA host gene 3 (SNHG3) in breast cancer remain largely undetermined.
  • Understanding lncRNA roles is crucial for identifying novel cancer biomarkers and therapeutic targets.

Purpose of the Study:

  • To investigate the role of SNHG3 in breast cancer initiation and progression.
  • To elucidate the underlying molecular mechanisms involving SNHG3 in breast cancer.
  • To evaluate SNHG3 as a potential therapeutic target for breast cancer treatment.

Main Methods:

  • Quantitative reverse transcription PCR (RT-qPCR) for SNHG3 expression analysis in breast cancer tissues and cell lines.
  • In vitro assays including Cell Counting Kit-8, colony formation, flow cytometry, wound-healing, and Matrigel invasion assays to assess cancer cell behaviors.
  • Luciferase reporter assays to determine the interaction between SNHG3 and miR-326.
  • In vivo studies using a nude mouse model to evaluate the effect of SNHG3 knockdown on tumor growth.

Main Results:

  • SNHG3 expression was significantly upregulated in breast cancer tissues and cell lines compared to normal controls.
  • Knockdown of SNHG3 suppressed breast cancer cell proliferation, colony formation, migration, and invasion in vitro.
  • Tumor growth in vivo was significantly delayed following SNHG3 knockdown.
  • SNHG3 functions as a competing endogenous RNA (ceRNA) for miR-326, a known tumor suppressor, with a strong negative correlation observed between their expression levels.
  • Inhibition of SNHG3 partially reversed the suppressive effects of miR-326 on cancer cell behaviors.

Conclusions:

  • SNHG3 acts as an oncogenic lncRNA in breast cancer by sponging miR-326, thereby promoting proliferation and metastasis.
  • SNHG3's role as a ceRNA highlights its potential as a novel therapeutic target for breast cancer intervention.
  • Further research into SNHG3-mediated pathways could lead to the development of targeted therapies for breast cancer patients.
Keywords:
SNHG3small nucleolar RNA host gene 3miR-326breast cancerproliferationinvasion

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