The HGF/SF-induced phosphorylation of paxillin, matrix adhesion, and invasion of prostate cancer cells were suppressed by NK4, an HGF/SF variant.

Parr, Christian, Davies, G., Nakamura, T., Matsumoto, Kei, Mason, Malcolm David ORCID: https://orcid.org/0000-0003-1505-2869 and Jiang, Wen Guo ORCID: https://orcid.org/0000-0002-3283-1111 2001. The HGF/SF-induced phosphorylation of paxillin, matrix adhesion, and invasion of prostate cancer cells were suppressed by NK4, an HGF/SF variant. Biochemical and Biophysical Research Communications 285 (5) , pp. 1330-1337. 10.1006/bbrc.2001.5307

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Abstract

Hepatocyte growth factor/scatter factor (HGF/SF) plays a crucial role in cancer cell migration, matrix adhesion, invasion, and angiogenesis, via the phosphorylation of the c-met tyrosine kinase. This study examined the ability of NK4, a recently discovered HGF/SF variant, to inhibit the influence of HGF/SF on cell-matrix interaction, paxillin phosphorylation, and invasion of prostate cancer cells. HGF/SF was shown to dramatically enhance tumour cell motility, invasion, cell-matrix adhesion, together with an increase in the degree of paxillin phosphorylation and formation of focal adhesion complexes. However, these HGF/SF-induced effects were suppressed by the presence of NK4. NK4 effectively inhibited the degree of HGF/SF-induced paxillin phosphorylation and matrix adhesion. As a consequence, the matrix invasion of these prostate cancer cells was also suppressed by NK4. In conclusion, this study shows that these HGF/SF-enhanced events, which are critical steps in metastasis, can be inhibited through the addition of NK4, thus warranting further in vivo studies on the implication of NK4 as a potential antimetastasis agent in prostate cancer.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Subjects:	R Medicine > R Medicine (General)
Uncontrolled Keywords:	hepatocyte growth factor/scatter factor (HGF/SF); paxillin; c-met proto-oncogene; NK4; focal adhesions
Publisher:	Elsevier
ISSN:	0006-291X
Last Modified:	01 Nov 2022 09:40
URI:	https://orca.cardiff.ac.uk/id/eprint/88817

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