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Cytotoxic necrotizing factor 1 promotes bladder cancer angiogenesis through activating RhoC.

Yaxiu Guo1, Jingyu Wang1, Kaichen Zhou1

  • 1Department of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Educational Ministry of China, Tianjin Key Laboratory of Cellular and Molecular Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 22, 2020
PubMed
Summary
This summary is machine-generated.

Uropathogenic Escherichia coli (UPEC) toxin CNF1 promotes bladder cancer by activating RhoC, which upregulates VEGF via HIF1α stabilization, driving angiogenesis. This pathway offers potential therapeutic targets for bladder cancer treatment.

Keywords:
RhoCangiogenesisbladder cancercytotoxic necrotizing factor 1uropathogenic Escherichia coli

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Area of Science:

  • Oncology
  • Microbiology
  • Molecular Biology

Background:

  • Uropathogenic Escherichia coli (UPEC) is linked to prostate and bladder cancers.
  • Cytotoxic necrotizing factor 1 (CNF1) is a key UPEC toxin, but its role in bladder cancer is unclear.

Purpose of the Study:

  • To investigate the role of CNF1 in bladder cancer progression.
  • To elucidate the molecular mechanisms by which CNF1 influences bladder cancer growth and angiogenesis.

Main Methods:

  • In vitro studies using bladder cancer cells to assess CNF1 effects on VEGF secretion and RhoC activation.
  • Investigated the role of RhoC, HIF1α, HSF1, and HSP90α in CNF1-mediated signaling.
  • In vivo studies using human bladder cancer xenografts to evaluate CNF1-induced angiogenesis and protein expression.

Main Results:

  • CNF1 activates RhoC, leading to increased vascular endothelial growth factor (VEGF) secretion and angiogenesis in bladder cancer.
  • CNF1-mediated RhoC activation stabilizes hypoxia-inducible factor 1α (HIF1α) by increasing heat shock protein 90α (HSP90α) expression.
  • Elevated HSP90α, HIF1α, and VEGF expression, along with increased angiogenesis, were observed in CNF1-treated xenografts and correlated with human bladder cancer development.

Conclusions:

  • CNF1 contributes to bladder cancer progression through the RhoC/HIF1α/VEGF pathway, promoting angiogenesis.
  • The findings suggest that CNF1-induced signaling represents a potential therapeutic target for bladder cancer.