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Inhibitory effects of H-Ras/Raf-1–binding affibody molecules on synovial cell function
KTH, School of Biotechnology (BIO), Protein Technology. KTH, School of Biotechnology (BIO), Centres, Albanova VinnExcellence Center for Protein Technology, ProNova.ORCID iD: 0000-0002-5391-600X
KTH, School of Biotechnology (BIO), Protein Technology. KTH, School of Biotechnology (BIO), Centres, Albanova VinnExcellence Center for Protein Technology, ProNova.ORCID iD: 0000-0003-4214-6991
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2014 (English)In: AMB Express, ISSN 2191-0855, E-ISSN 2191-0855, Vol. 4, no 82Article in journal (Refereed) Published
Abstract [en]

Affibody molecules specific for H-Ras and Raf-1 were evaluated for their ability to inhibit synovial cell function. Affibody molecules targeting H-Ras (Zras122, Zras220, and Zras521) or Raf-1 (Zraf322) were introduced into the MH7A synovial cell line using two delivery methods: transfection with plasmids encoding the affibody molecules or direct introduction of affibody protein using a cell-penetrating peptide reagent. Interleukin-6 (IL-6) and prostaglandin E2 (PGE2) production by MH7A cells were analyzed by enzyme-linked immunosorbent assay after stimulation with tumor necrosis factor-alpha (TNF-α). Cell proliferation was also analyzed. Phosphorylation of extracellular signal-regulated kinase (ERK) was analyzed by western blot. All affibody molecules could inhibit IL-6 and PGE2 production in TNF-α-stimulated MH7A cells. The inhibitory effect was stronger when affibody molecules were delivered as proteins via a cell-penetrating peptide reagent than when plasmid-DNA encoding the affibody moelcules was transfected into the cells. Plasmid-expressed Zras220 inhibited phosphorylation of ERK in TNF-α-stimulated MH7A cells. Protein-introduced Zraf322 inhibited the production of IL-6 and PGE2 and inhibited cell proliferation in MH7A cells. These findings suggest that affibody molecules specific for H-Ras and Raf-1 can affect intracellular signal transduction through the MAP kinase pathway to inhibit cell proliferation and production of inflammatory mediators by synovial cells.

Place, publisher, year, edition, pages
Springer Berlin/Heidelberg, 2014. Vol. 4, no 82
Keyword [en]
affinity cancer
National Category
Biological Sciences
Research subject
Biotechnology
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URN: urn:nbn:se:kth:diva-164186DOI: 10.1186/s13568-014-0082-3ISI: 000358068500001Scopus ID: 2-s2.0-84957590363OAI: oai:DiVA.org:kth-164186DiVA: diva2:804974
Note

QC 20150420

Available from: 2015-04-14 Created: 2015-04-14 Last updated: 2017-12-04Bibliographically approved

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Gräslund, TorbjörnNygren, Per-Åke

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