Changes in cell adhesion proteins induced by the treatment with cisplatin and their role in cisplatin-resistance (CROSBI ID 542382)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija
Podaci o odgovornosti
Osmak, Maja ; Brozović, Anamaria ; Čimbora Zovko, Tamara ; Majhen, Dragomira ; Fritz, Gerhard ; Ambriović Ristov, Andreja
engleski
Changes in cell adhesion proteins induced by the treatment with cisplatin and their role in cisplatin-resistance
Greater insight into the molecular mechanisms regarding modulation of the cellular response to anti-cancer drugs could help to optimize therapeutic strategies. New data suggest the possible role of cell adhesion proteins in drug-resistance. From laryngeal carcinoma HEp2 cells, we have developed cDDP-resistant CA3ST (by cDDP acute treatment) and CK2 (by cDDP chronic treatment) sublines which exhibited altered cell adhesion to extracellular matrix and altered formation of cell-cell junctions comparing to their parental cells. In CA3ST cells we found increased expression of  v 3 integrin and coxsackie adenovirus receptor (CAR). Conversely, in CK2 cells the expression of  v 3 integrin was similar to HEp2, while the expression of CAR was slightly decreased. Both, CA3ST and CK2 sublines showed similar alterations in cell-cell junction proteins, i.e. increased expression of  -catenin and decreased expression of plakoglobin, while the expression of N-cadherin, p120 catenin and desmoglein was similar as compared to HEp2 cells. The isolation of  v 3-expressing stable transfectants from HEp2 cells expressing increased amount of  v 3 integrin, confirmed its role in resistance. However, in HEp2-derived CAR-expressing clones no correlation between CAR expression and cDDP-resistance was found. To show the causative relationship between the pattern of plakoglobin/β -catenin expression and resistance, we overexpressed plakoglobin in CA3ST cells ; yet none of the clones, showing similar plakoglobin/β -catenin pattern to HEp2 cells, restored sensitivity to cisplatin. Thus, increased expression of  v 3 is very likely one of the mechanisms involved in cDDP-resistance. On the contrary, the changes in expression of CAR, plakoglobin and β -catenin expression are presumably a secondary event of cellular response triggered by cisplatin. Therefore, different treatment schedule used for resistance development had induced different alterations in these cells, which are reflected in different resistance-mechanisms.
cisplatin; resistance; cell adhesion; integrins; cadherins; catenins
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Podaci o prilogu
S61-S61.
2008.
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objavljeno
Podaci o matičnoj publikaciji
Abstracts of the 13th World Congress on Advances in Oncology, and 11th International Symposium on Molecular Medicine ; u: International Journal of Molecular Medicine. Supplement
Spandidos, D.A.
Atena: Lychnia, Greece
Podaci o skupu
The 13th World Congress on Advances in Oncology and 11th International Symposium on Molecular Medicine
pozvano predavanje
09.10.2008-11.10.2008
Hersonissos, Grčka