As both HC11-HSP90α HC11-HSP90αbehaved similarly, we used only line two for further cellacterisation.
In both cell lines, cell growth/proliferation was stimulated by Ca2+ or calcimimetic NPS R-467 addition and their effects were reversed by the CaSR antagonist NPS 2390 even if the two cell lines behaved differently.
Since all cell lines behaved similarly in this respect, we selected SK-N-MC cells as a model for further characterization of the mechanisms underlying the telomere shortening induced sensitization of cancer cells to chemotherapy and the differential sensitivity to cisplatinum.
The three cell lines behaved similarly [see additional data file 4].
Again, transformed cell lines behaved differentially; in CCL-51 and U-2 OS, GGPP rescued ibandronate attenuated cell multiplication, up regulated DNMT1 and, consequently, down regulated FAS expression.
During the course of 24 hrs postradiation exposure, the three cell lines behaved differently in terms of the persistence and/or removal of the γ-H2AX foci.
However, in vivo, in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors.
The two cell lines behaved similarly, and Figures 5(A) and 5(B) show their response to biguanide concentrations equal to one tenth of their isolated complex I IC50 values.
Since it was shown (Hinz et al, 2000; Trauzold et al, 2001) that pancreatic tumour cell lines behave like type II cells in both, CD95- and TRAIL-mediated apoptosis, we did not only analyse the expression levels of caspases and DISC components, but also of proteins which participate in the mitochondrial apoptosis pathway.
Specifically, mice and rats have placentas which differ from the human both in structure and at the molecular level [ 3]; in addition, the human placental cell lines behave differently in culture, compared to the placental cells as they exist "in vivo" in the pregnant patient [ 4].
