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2015 ; 5
(ä): 10356
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English Wikipedia
TP53 transcription factor for the NEDD9/HEF1/Cas-L gene: potential targets in
Non-Small Cell Lung Cancer treatment
#MMPMID26011298
Rousseau B
; Jacquot C
; Le Palabe J
; Malleter M
; Tomasoni C
; Boutard T
; Sakanyan V
; Roussakis C
Sci Rep
2015[May]; 5
(ä): 10356
PMID26011298
show ga
Lung cancer is a serious public health problem. Although there has been
significant progress in chemotherapy, non-small cell lung cancer is still
resistant to current treatments, primarily because of the slow rate of cell
development. It is thus important to find new molecules directed against targets
other than proliferation agents. Considering the high proportion of mutant
proteins in tumor cells, and the high rate of mutation of the TP53 gene in all
cancers, and in NSCLC in particular, this gene is a perfect target. Certain new
molecules have been shown to restore the activity of mutated p53 protein, for
example PRIMA-1, which reactivates the His273 mutant p53. In a previous study, we
presented triazine A190, a molecule with a cytostatic activity that blocks cells
in the G1 phase and induces apoptosis. Here, we show that A190 not only restores
mutant p53 activity, but also induces an overexpression of the NEDD9 gene,
leading to apoptotic death. These findings might offer hope for the development
of new targeted therapies, specific to tumor cells, which spare healthy cells.
|Adaptor Proteins, Signal Transducing/antagonists &
inhibitors/genetics/*metabolism
[MESH]