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Fetal colon cell line FHC exhibits tumorigenic phenotype, complex karyotype, and TP53 gene mutation
Karel Souček, Pavla Gajdušková, Marie Brázdová, Martina Hýžd'alová, Lenka Kočí, David Vydra, Radek Trojanec, Zuzana Pernicová, Lenka Lentvorská, Marián Hajdúch, Jiřina Hofmanová, Alois Kozubík
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NS9600
MZ0
CEP - Centrální evidence projektů
- MeSH
- apoptóza fyziologie MeSH
- buněčná adheze fyziologie MeSH
- buňky - růstové procesy fyziologie MeSH
- cytogenetické vyšetření metody MeSH
- fenotyp MeSH
- geny p53 MeSH
- HCT116 buňky MeSH
- hybridizace in situ fluorescenční MeSH
- karcinoembryonální antigen metabolismus MeSH
- karyotypizace MeSH
- keratiny metabolismus MeSH
- kolon cytologie metabolismus fyziologie MeSH
- lidé MeSH
- mutační analýza DNA metody MeSH
- myši SCID MeSH
- myši MeSH
- nádorová transformace buněk genetika patologie MeSH
- nádory tračníku genetika patologie MeSH
- plod cytologie MeSH
- poškození DNA MeSH
- signální transdukce MeSH
- srovnávací genomová hybridizace MeSH
- transformované buněčné linie MeSH
- transplantace nádorů MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Stable cell lines obtained by spontaneous immortalization might represent early stages of malignant transformation and be useful experimental models for studies of mechanisms of cancer development. The FHC (fetal human cells) cell line has been established from normal fetal colonic mucosa. Detailed characterization of this cell line and mechanism of spontaneously acquired immortality have not been described yet. Therefore, we characterized the FHC cell line in terms of its tumorigenicity, cytogenetics, and TP53 gene mutation analysis. FHC cells displayed capability for anchorage-independent growth in semisolid media in vitro and formed solid tumors after transplantation into SCID (severe combined immunodeficiency) mice. This tumorigenic phenotype was associated with hypotriploidy and chromosome number ranging from 66 to 69. Results of comparative genetic hybridization arrays showed that most chromosomes included regions of copy number gains or losses. Region 8q23 approximately 8q24.3 (containing, e.g., MYC proto-oncogene) was present in more than 20 copies per nucleus. Moreover, we identified mutation of TP53 gene in codon 273; triplet CGT coding Arg was changed to CAG coding His. Expression of Pro codon 72 polymorphic variant of p53 was also detected. Mutation of TP53 gene was associated with abolished induction of p21(Waf1/Cip1) and MDM-2 proteins and resistance to apoptosis after genotoxic treatment. Because of their origin from normal fetal colon and their relative resistance to the induction of apoptosis, FHC cells can be considered a valuable experimental model for various studies.
Citace poskytuje Crossref.org
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- $a Stable cell lines obtained by spontaneous immortalization might represent early stages of malignant transformation and be useful experimental models for studies of mechanisms of cancer development. The FHC (fetal human cells) cell line has been established from normal fetal colonic mucosa. Detailed characterization of this cell line and mechanism of spontaneously acquired immortality have not been described yet. Therefore, we characterized the FHC cell line in terms of its tumorigenicity, cytogenetics, and TP53 gene mutation analysis. FHC cells displayed capability for anchorage-independent growth in semisolid media in vitro and formed solid tumors after transplantation into SCID (severe combined immunodeficiency) mice. This tumorigenic phenotype was associated with hypotriploidy and chromosome number ranging from 66 to 69. Results of comparative genetic hybridization arrays showed that most chromosomes included regions of copy number gains or losses. Region 8q23 approximately 8q24.3 (containing, e.g., MYC proto-oncogene) was present in more than 20 copies per nucleus. Moreover, we identified mutation of TP53 gene in codon 273; triplet CGT coding Arg was changed to CAG coding His. Expression of Pro codon 72 polymorphic variant of p53 was also detected. Mutation of TP53 gene was associated with abolished induction of p21(Waf1/Cip1) and MDM-2 proteins and resistance to apoptosis after genotoxic treatment. Because of their origin from normal fetal colon and their relative resistance to the induction of apoptosis, FHC cells can be considered a valuable experimental model for various studies.
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