@Article{,
AUTHOR = {S. Wittnebel, A. Jalil, J. Thiery, S. DaRocha, E. Viey, B. Escudier, S. Chouaib, A. Caignard},
TITLE = {The sensitivity of renal cell carcinoma cells to interferon alpha correlates with p53-induction and involves Bax},
JOURNAL = {European Cytokine Network},
VOLUME = {16},
YEAR = {2005},
NUMBER = {2},
PAGES = {123--127},
URL = {http://www.techscience.com/ECN/v16n2/66224},
ISSN = {1952-4005},
ABSTRACT = {Interferon alpha (IFN-α) is an approved treatment in metastatic renal cell carcinoma (RCC). The
underlying mechanisms are far from being clear, but are presumed to be a combination of stimulation of
cell-mediated cytotoxicity, direct antiproliferative activity and antiangiogenic effects. Recently, the role of p53 in
the cellular response to IFN-α has been proposed in other tumor models (hepatoblastoma). We therefore studied
the expression of p53 during IFN-α treatment using two freshly established RCC cell lines RCC5 and RCC7.
While IFN-α treatment significantly enhanced the expression of p53 in RCC7, no changes were observed in RCC5.
Cell viability under IFN-α remained unchanged in both cell lines. Following γ-irradiation, a p53-activating
stimulus, an enhanced cell death was observed in IFN-α-treated RCC7 but not in RCC5. We further demonstrate
that there were no changes in Bcl-2- and Bax-expression, two target genes regulated by p53. However,
intracellular staining revealed that cell death induced by IFN-α and γ-irradiation was preceded by a shift of Bax
to the mitochondria in RCC7. Our results suggest a role of p53 and its downstream target Bax, in the control of
RCC sensitivity to IFN-α.},
DOI = {}
}