Ontology type: schema:ScholarlyArticle
2002-11
AUTHORSEun-Young Shin, Eun-Kyung Ma, Chi-Kyung Kim, Sahng-June Kwak, Eung-Gook Kim
ABSTRACTPURPOSE: We investigated the signaling pathway for keratinocyte growth factor (KGF)-induced invasion using human stomach cancer cell line, SNU-16. METHODS: Alterations in the activities of Src, extracellular signal-regulated kinase (ERK), and phospholipase D (PLD) were measured using [gamma-(32)P] ATP for autophosphorylation of Src, phospho-specific ERK antibody, and [9,10-(3)H] myristic acid, respectively, while herbimycin A, PD98059 and butan-1-ol were used to inhibit their activities. Matrix metalloproteases (MMPs) and urokinase-type plasminogen activator (uPA) were quantified with zymography and Matrigel-coated Transwell was employed to estimate the invasiveness of SNU-16 cells. RESULTS: Src, ERK, and PLD were activated in response to KGF treatment, and inhibition of these enzymes - by their specific inhibitors - decreased KGF-induced invasion in a dose-dependent manner. However, only inhibition of Src and ERK could block KGF-stimulated secretion of uPA and MMP-9. CONCLUSION: Src, ERK, and PLD are suggested as mediators of KGF-induced invasion in SNU-16. uPA and MMP-9 are considered as downstream targets of Src and ERK whereas PLD is thought to utilize different pathways. More... »
PAGES596-602
http://scigraph.springernature.com/pub.10.1007/s00432-002-0388-4
DOIhttp://dx.doi.org/10.1007/s00432-002-0388-4
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/12458339
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