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. 2021 Dec 29;23(1):337. doi: 10.3390/ijms23010337

Table 1.

Various model systems studying the involvement of urokinase-type plasminogen activator (uPA) in angiogenesis.

Model Outcome Mechanism
uPA and uPAR deficient mice implanted with murine prostate cancer cells
  • -

    Substantial decrease in tumor volume.

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    Significant reduction in angiogenesis.

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    Tumors showed significantly fewer infiltrating macrophages

 Reduced tumor size in uPA and uPAR deficient mice could be due to the reduction of macrophage number [49]
Stable transfection of SNB19 cells with antisense-uPA
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    Downregulation of uPA and cellular migration.

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    Cell cycle arrest in G2/M and interrupted actin cytoskeleton development.

 uPa deficiency decreased PI3K and Akt phosphorylation and actin cytoskeleton formation [50]
uPA deficient mice implanted with malignant murine keratinocytes
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    Normal tumor angiogenesis.

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    Increase in tPA activity at the tumor site.

 uPA deficiency was recompensed by tPA [51]
MCF-7 cells treated with single-chained uPA (scuPA) and uPA amino-terminal fragment (ATF)
  • -

    Increased cell migration

 scuPA and uPA ATF
induced the Phosphorylation and activation of ERK1/2 [57]