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MicroRNA-377 suppresses initiation and progression of esophageal cancer by inhibiting CD133 and VEGF

B Li1,2,3, W W Xu1,2, L Han1,2

  • 1School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, China.

Oncogene
|March 14, 2017
PubMed

Insights

MicroRNA-377 (miR-377) is downregulated in esophageal squamous cell carcinoma (ESCC). Restoring miR-377 inhibits ESCC growth and metastasis, suggesting its potential as a diagnostic biomarker and therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Esophageal cancer, particularly ESCC, has poor survival rates and limited treatment options.
  • MicroRNAs (miRNAs) are emerging as critical regulators in cancer development.
  • The role of miR-377 in ESCC remains largely unexplored despite its location on a frequently deleted chromosome region.

Purpose of the Study:

  • To investigate the biological functions, clinical significance, and therapeutic potential of miR-377 in esophageal squamous cell carcinoma (ESCC).
  • To determine the correlation between miR-377 expression levels and patient survival, tumor stage, metastasis, and treatment response.
  • To elucidate the molecular mechanisms by which miR-377 affects ESCC initiation and progression.

Main Methods:

  • Quantitative analysis of miR-377 expression in ESCC tumor tissues and patient serum.
  • Correlation analysis between miR-377 levels and clinical parameters (survival, tumor stage, metastasis, treatment resistance).
  • In vitro and in vivo experiments to assess the effects of miR-377 overexpression and silencing on ESCC cell behavior and tumor growth.
  • Mechanistic studies involving direct binding analysis of miR-377 to target genes (CD133, VEGF).
  • Evaluation of systemic delivery of miR-377 mimics in a mouse model.

Main Results:

  • miR-377 expression was significantly downregulated in ESCC tumor tissues and serum.
  • Lower miR-377 levels correlated with poorer patient survival, advanced tumor stage, metastasis, and chemoradiotherapy resistance.
  • Overexpression of miR-377 inhibited ESCC initiation, growth, angiogenesis, and metastasis in vitro and in vivo.
  • miR-377 directly targets and regulates CD133 and VEGF.
  • Systemic delivery of miR-377 mimic suppressed tumor growth, angiogenesis, and lung metastasis in mice without significant toxicity.

Conclusions:

  • miR-377 functions as a tumor suppressor in ESCC by inhibiting initiation, progression, and metastasis.
  • miR-377 holds promise as a non-invasive diagnostic and prognostic biomarker for ESCC.
  • Restoring miR-377 levels represents a potential therapeutic strategy for ESCC patients.

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