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GGTase-I deficiency...
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Sjögren, Anna-Karin,1980Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine
(author)
GGTase-I deficiency reduces tumor formation and improves survival in mice with K-RAS-induced lung cancer
- Article/chapterEnglish2007
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LIBRIS-ID:oai:gup.ub.gu.se/45364
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https://gup.ub.gu.se/publication/45364URI
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https://doi.org/10.1172/JCI30868DOI
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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Protein geranylgeranyltransferase type I (GGTase-I) is responsible for the posttranslational lipidation of CAAX proteins such as RHOA, RAC1, and cell division cycle 42 (CDC42). Inhibition of GGTase-I has been suggested as a strategy to treat cancer and a host of other diseases. Although several GGTase-I inhibitors (GGTIs) have been synthesized, they have very different properties, and the effects of GGTIs and GGTase-I deficiency are unclear. One concern is that inhibiting GGTase-I might lead to severe toxicity. In this study, we determined the effects of GGTase-I deficiency on cell viability and K-RAS-induced cancer development in mice. Inactivating the gene for the critical beta subunit of GGTase-I eliminated GGTase-I activity, disrupted the actin cytoskeleton, reduced cell migration, and blocked the proliferation of fibroblasts expressing oncogenic K-RAS. Moreover, the absence of GGTase-I activity reduced lung tumor formation, eliminated myeloproliferative phenotypes, and increased survival of mice in which expression of oncogenic K-RAS was switched on in lung cells and myeloid cells. Interestingly, several cell types remained viable in the absence of GGTase-I, and myelopoiesis appeared to function normally. These findings suggest that inhibiting GGTase-I may be a useful strategy to treat K-RAS-induced malignancies.
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Andersson, Karin,1972Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xankar
(author)
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Liu, Meng,1976Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xliume
(author)
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Cutts, Briony,1976Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xcutbr
(author)
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Karlsson, Christina,1956Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xkarlc
(author)
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Wahlström, Annika,1975Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xsannj
(author)
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Dalin, Martin,1982Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine(Swepub:gu)xdalim
(author)
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Weinbaum, C.
(author)
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Casey, P. J.
(author)
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Tarkowski, Andrej,1951Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research(Swepub:gu)xtaand
(author)
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Swolin, Birgitta,1939Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för klinisk kemi och transfusionsmedicin,Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine(Swepub:gu)xswobi
(author)
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Young, S. G.
(author)
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Bergö, Martin,1970Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xbmarl
(author)
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Göteborgs universitetInstitutionen för medicin, avdelningen för invärtesmedicin
(creator_code:org_t)
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In:J Clin Invest117:5, s. 1294-3040021-9738
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Liu, Meng, 1976
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Weinbaum, C.
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