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A disintegrin-like and metalloproteinase 15 facilitates glioblastoma proliferation and metastasis through activation

Rong Ren1, Zuowei Li2,3,4, Qiong Fang5

  • 1Department of Traditional Chinese Medicine, Qingdao Chengyang People's Hospital, Qingdao, Shandong, China.

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|April 22, 2025
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Summary

A disintegrin-like and metalloproteinase 15 (ADAM15) promotes glioblastoma progression by upregulating protease-activated receptor 1 (PAR1). Inhibiting PAR1 significantly reduces glioblastoma cell proliferation, migration, and invasion.

Keywords:
A disintegrin-like and metalloproteinase domain 15Epithelial-mesenchymal transitionProtease-activated receptor 1glioblastoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Glioblastoma is an aggressive brain tumor with poor prognosis.
  • ADAM15 and PAR1 are implicated in cancer progression, influencing cell adhesion, migration, and tumorigenesis.

Purpose of the Study:

  • To investigate the interaction between ADAM15 and PAR1 in modulating epithelial-mesenchymal transition (EMT) in glioblastoma.
  • To explore the potential of targeting ADAM15-PAR1 interaction as a therapeutic strategy.

Main Methods:

  • Overexpression of ADAM15 in glioblastoma cell lines (U251, U87).
  • Assays for proliferation, invasion, migration, and EMT markers (Transwell, EdU, clonogenic, Ki67, Western blot, qRT-PCR).
  • Inhibition of PAR1 and PAR2 signaling pathways.

Main Results:

  • ADAM15 overexpression significantly enhanced glioblastoma cell migration, invasion, and proliferation.
  • ADAM15 overexpression led to increased expression of PAR1 and EMT markers.
  • PAR1 inhibition suppressed glioblastoma cell proliferation, migration, invasion, and EMT, while PAR2 inhibition had no significant effect.

Conclusions:

  • ADAM15 drives glioblastoma progression, at least in part, through the PAR1 signaling pathway.
  • Targeting PAR1 represents a potential therapeutic avenue for glioblastoma treatment.