PML and TRF2 protein expression in hereditary and sporadic colon cancer
Jazyk angličtina Země Slovensko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
17822315
Knihovny.cz E-zdroje
- MeSH
- adaptorové proteiny signální transdukční genetika MeSH
- DNA nádorová MeSH
- dospělí MeSH
- homolog 2 proteinu MutS genetika MeSH
- jaderné proteiny genetika metabolismus MeSH
- kolorektální nádory genetika metabolismus patologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikrosatelitní nestabilita * MeSH
- mikrosatelitní repetice MeSH
- mucinózní adenokarcinom genetika metabolismus patologie MeSH
- MutL homolog 1 MeSH
- nádorové buňky kultivované MeSH
- nádorové proteiny metabolismus MeSH
- nádorové supresorové proteiny metabolismus MeSH
- nádory genetika metabolismus patologie MeSH
- polymerázová řetězová reakce MeSH
- protein promyelocytické leukemie MeSH
- protein TRF2 metabolismus MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- telomerasa metabolismus MeSH
- telomery fyziologie MeSH
- transkripční faktory metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adaptorové proteiny signální transdukční MeSH
- DNA nádorová MeSH
- homolog 2 proteinu MutS MeSH
- jaderné proteiny MeSH
- MLH1 protein, human MeSH Prohlížeč
- MSH2 protein, human MeSH Prohlížeč
- MutL homolog 1 MeSH
- nádorové proteiny MeSH
- nádorové supresorové proteiny MeSH
- PML protein, human MeSH Prohlížeč
- protein promyelocytické leukemie MeSH
- protein TRF2 MeSH
- telomerasa MeSH
- TERT protein, human MeSH Prohlížeč
- transkripční faktory MeSH
The PML (promyelocytic leukemia) protein is concentrated in the PML nuclear bodies. In human cell lines and tumors maintaining their telomeres by alternative lengthening (ALT), the PML protein is colocalized with TRF2 and several other proteins in the so called ALT-associated PML bodies. The aim of this study was to determine if there is any difference in PML protein expression between tumors with stable microsatellites (MSS) and those with high-frequency microsatellite instability (MSI-H), if PML protein expression might be a prognostic factor and if MSI-H tumors more frequently use alternative lengthening of telomeres measured by the presence of ALT-associated PML bodies. Eighty colorectal cancer samples (32 MSI-H and 48 MSS) and 8 human tumor cell lines (Saos-2, U2OS, DU145, LNCaP, U87, HeLa, MCF7 and T98G) were included into the study. Double-colour immunofluorescence staining was used. Downregulation of PML protein expression was found in 7 of 32 (22%) MSI-H and 11 of 48 (23%) MSS tumors (p=0.520). There was no correlation between PML expression and age, histological typing, localization of the tumor in colon, TNM classification, disease-free and overall survival. The Saos-2 and U2OS (ALT using cell lines) and the MCF7 (active telomerase) cell line were characterized by the presence of ALT-associated PML bodies; no such bodies were detected in the DU145, LNCaP, U87, HeLa and T98G cell lines (active telomerase); accumulation of TRF2 was absent or much weaker in these cell lines compared to Saos-2 or U2OS. Accumulation of the TRF2 protein was detected in 16 of 80 (20%) tumors and PML and TRF2 colocalization in 2 MSI-H tumors (6%). In conclusion, the PML protein was downregulated in approximately 20% of tumors; there was no difference between MSS and MSI-H tumors. PML protein expression does not seem to be a prognostic factor.