Παρακαλώ χρησιμοποιήστε αυτό το αναγνωριστικό για να παραπέμψετε ή να δημιουργήσετε σύνδεσμο προς αυτό το τεκμήριο:
https://hdl.handle.net/10442/7319
Εξειδίκευση τύπου : | Άρθρο σε επιστημονικό περιοδικό |
Τίτλος: | Deregulated overexpression of hCdt1 and hCdc6 promotes malignant behavior |
Δημιουργός/Συγγραφέας: | Liontos, Michalis Koutsami, Marilena Sideridou, Maria Evangelou, Konstantinos Kletsas, Dimitris Levy, Brynn Kotsinas, Athanassios Nahum, Odelia [EL] Ζουμπουρλής, Βασίλης[EN] Zoumpourlis, Vassilis Kouloukoussa, Mirsini Lygerou, Zoi Taraviras, Stavros Kittas, Christos Bartkova, Jirina Papavassiliou, Athanasios G. Bartek, Jiri Halazonetis, Thanos D. Gorgoulis, Vassilis G. |
Ημερομηνία: | 2007-11-15 |
Γλώσσα: | Αγγλικά |
DOI: | 10.1158/0008-5472.can-07-2837 |
Περίληψη: | The accurate execution of DNA replication requires a strict control of the replication licensing factors hCdt1 and hCdc6. The role of these key replication molecules in carcinogenesis has not been clarified. To examine how early during cancer development deregulation of these factors occurs, we investigated their status in epithelial lesions covering progressive stages of hyperplasia, dysplasia, and full malignancy, mostly from the same patients. Abnormal accumulation of both proteins occurred early from the stage of dysplasia. A frequent cause of unregulated hCdc6 and hCdt1 expression was gene amplification, suggesting that these components can play a role per se in cancer development. Overexpression of hCdt1 and hCdc6 promoted rereplication and generated a DNA damage response, which activated the antitumor barriers of senescence and apoptosis. Generating an inducible hCdt1 cellular system, we observed that continuous stimulus by deregulated hCdt1 led to abrogation of the antitumor barriers and resulted in the selection of clones with more aggressive properties. In addition, stable expression of hCdc6 and hCdt1 in premalignant papilloma cells led to transformation of the cells that produced tumors upon injection into nude mice depicting the oncogenic potential of their deregulation. |
Τίτλος πηγής δημοσίευσης: | Cancer Research |
Τόμος/Κεφάλαιο: | 67 |
Τεύχος: | 22 |
Σελίδες: | 10899-10909 |
Θεματική Κατηγορία: | [EL] Εσωτερική ιατρική[EN] Internal medicine |
Λέξεις-Κλειδιά: | Neoplasms. Tumors. Oncology |
Κάτοχος πνευματικών δικαιωμάτων: | © 2007 American Association for Cancer Research |
Σημειώσεις: | http://cancerres.aacrjournals.org/ http://cancerres.aacrjournals.org/cgi/reprint/67/22/10899?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&volume=67&firstpage=10899&resourcetype=HWCIT |
ΙΒΦΧΒ: αρχειακή συλλογή: | Ινστιτούτο Βιολογικών Ερευνών και Βιοτεχνολογίας (ΙΒΕΒ) (έως 2012) |
Εμφανίζεται στις συλλογές: | Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο
|