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DDX5 Silencing Suppresses the Migration of Basal cell Carcinoma Cells by Downregulating JAK2/STAT3 Pathway

Zhe Quan1, Bei-Bei Zhang1, Fang Yin1

  • 1Department of Dematology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Technology in Cancer Research & Treatment
|December 25, 2019
PubMed

Insights

DEAD (Asp-Glu-Ala-Asp) box protein 5 promotes basal cell carcinoma growth and invasion. Inhibiting this protein and the JAK2/STAT3 pathway may offer new therapeutic strategies for basal cell carcinoma.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Basal cell carcinoma (BCC) pathogenesis involves aberrant hedgehog signaling.
  • DEAD (Asp-Glu-Ala-Asp) box protein 5 (DDX5) is overexpressed in cancers, correlating with tumor progression.

Purpose of the Study:

  • To investigate the role of DDX5 in BCC cell growth, migration, and invasion.
  • To explore the association between DDX5 and the JAK2/STAT3 pathway in BCC.

Main Methods:

  • Quantitative real-time PCR and Western blot to assess DDX5 expression.
  • Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay for apoptosis.
  • Analysis of JAK2/STAT3 pathway modulation following DDX5 knockdown and JAK2 inhibition.

Main Results:

  • DDX5 is significantly overexpressed in BCC cells.
  • DDX5 knockdown suppressed BCC cell migration and invasion and enhanced tunicamycin-induced apoptosis.
  • DDX5 silencing upregulated JAK2 and STAT3 expression; JAK2 inhibition reduced STAT3 levels and reversed DDX5 knockdown's anti-migratory/invasive effects.

Conclusions:

  • DDX5 promotes BCC cell proliferation, migration, and invasion.
  • DDX5 may exert its effects by modulating the JAK2/STAT3 pathway.
  • DDX5 represents a potential therapeutic target for BCC treatment via JAK2/STAT3 pathway downregulation.
Keywords:
BCCDDX5JAK2STAT3invasionmigration

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