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  1. Home
  3. S100a10 Promotes Hcc Development And Progression Via Transfer In Extracellular Vesicles And Regulating Their Protein Cargos.
  1. Home
  3. S100a10 Promotes Hcc Development And Progression Via Transfer In Extracellular Vesicles And Regulating Their Protein Cargos.

Related Experiment Video

An Enrichment Method for Small Extracellular Vesicles Derived from Liver Cancer Tissue
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S100A10 promotes HCC development and progression via transfer in extracellular vesicles and regulating their protein

Xia Wang1,2, Hongyang Huang1,2, Karen Man-Fong Sze1,2

  • 1Department of Pathology, University of Hong Kong Faculty of Medicine, Hong Kong, Hong Kong.

Gut
|January 11, 2023

View abstract on PubMed

Summary
This summary is machine-generated.

S100 calcium binding protein A10 (S100A10) promotes hepatocellular carcinoma (HCC) progression by transferring via extracellular vesicles (EVs). Blocking EV-S100A10 may offer a therapeutic strategy for HCC.

Keywords:
HEPATOCELLULAR CARCINOMAMOLECULAR MECHANISMSMOLECULAR ONCOLOGY

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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Tumor cells often resemble their progenitor cells, with S100 calcium binding protein A10 (S100A10) showing expression patterns similar to liver progenitor genes.
  • The role of S100A10 in hepatocellular carcinoma (HCC) progression remains unclear.
  • Extracellular vesicles (EVs) are key in tumor development and metastasis, but the extracellular functions of S100A10, especially within EVs (EV-S100A10), are unknown.

Purpose of the Study:

  • To investigate the functions and mechanisms of S100A10 and EV-S100A10 in HCC progression.
  • To evaluate the therapeutic potential of targeting EV-S100A10.

Main Methods:

  • In vitro and in vivo studies were conducted to analyze S100A10 and EV-S100A10 functions.
  • Neutralizing antibody (NA) against S100A10 was employed to assess the impact of EV-S100A10.

Main Results:

  • S100A10 enhanced HCC initiation, self-renewal, chemoresistance, and metastasis.
  • S100A10 was secreted by HCC cells into EVs and found in the plasma of HCC patients.
  • EV-S100A10 promoted HCC stemness and metastasis, upregulated EGFR, AKT, and ERK signaling, and induced epithelial-mesenchymal transition.
  • S100A10-enveloped EVs acted as chemoattractants and modulated EV protein cargo, including MMP2, fibronectin, and EGF, via integrin αV binding.
  • Neutralization of EV-S100A10 significantly reduced these pro-tumorigenic effects.

Conclusions:

  • S100A10 promotes HCC progression through EV-mediated transfer and regulation of EV protein cargo.
  • EV-S100A10 presents a potential therapeutic target and a biomarker for HCC progression.