Suppression of cell growth by wild-type p53 in tumor-derived rat esophageal epithelial cells

1996 ◽  
Author(s):  
D Wang ◽  
J Lang ◽  
C Weghorst ◽  
C Sabourin ◽  
G Stoner
Keyword(s):  
Cell Growth ◽  
Epithelial Cells ◽  
Wild Type ◽  
Wild Type P53 ◽  
Esophageal Epithelial Cells

scholarly journals Tolerance of high levels of wild-type p53 in transformed epithelial cells dependent on auto-regulation by mdm-2

Oncogene ◽  
1997 ◽  
Vol 14 (15) ◽  
pp. 1859-1868 ◽  
Author(s):  
Jeremy P Blaydes ◽  
Véronique Gire ◽  
Janet M Rowson ◽  
David Wynford-Thomas
Keyword(s):  
Epithelial Cells ◽  
Wild Type ◽  
Wild Type P53

scholarly journals Myc supercompetitor cells exploit the NMDA receptor to subdue their wild-type neighbours via cell competition

2020 ◽  
Author(s):  
Agnes R. Banreti ◽  
Pascal Meier
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Cell Growth ◽  
Epithelial Cells ◽  
Fitness Landscape ◽  
Dependent Manner ◽  
Wild Type ◽  
Direct Inhibition ◽  
Cell Competition ◽  
Competitive Behaviour

SUMMARYMyc is a major driver of cell growth in many cancers, but direct inhibition of Myc’s oncogenic activity has been challenging. Interactions between wild-type and Myc-expressing cells cause Myc cells to acquire ‘supercompetitor’ behaviour that increases their fitness and enables them to overtake the tissue by killing their wild-type neighbours through TNF-induced cell death during a process called cell competition. Here we report that the competitive behaviour of Myc, RasV12 cells, and normal epithelial cells, critically depends on the NMDA receptor. Myc cells upregulate NMDAR2 (NR2) to gain supercompetitor status and subdue their wild-type neighbours. Pharmacological inhibition or genetic depletion of NR2 changes the supercompetitor status of oncogenic Myc or RasV12 clones into ‘superlosers’, resulting in their elimination via cell competition by wild-type neighbours in a TNF-dependent manner. Our data demonstrate that that the NMDA receptor (NMDAR) determines cellular fitness during cell competition, and can be targeted to change the fitness landscape of supercompetitive Myc and RasV12 clones, converting them into superlosers.

Possible Involvement of bcl-2 Suppression in Wild-Type p53 Gene-Dependent Cell Growth Repression in Rat Osteosarcoma Cells

2000 ◽  
Vol 28 (4) ◽  
pp. 575-579 ◽  
Author(s):  
Kanya Honoki ◽  
Toshifumi Tsujiuchi ◽  
Masahiro Tsutsumi ◽  
Akira Kido ◽  
Toru Morishita ◽  
...  
Keyword(s):  
Cell Growth ◽  
P53 Gene ◽  
Wild Type ◽  
Osteosarcoma Cells ◽  
Dependent Cell ◽  
Wild Type P53

Trisubstituted and tetrasubstituted pyrazolines as a novel class of cell-growth inhibitors in tumor cells with wild type p53

2013 ◽  
Vol 21 (23) ◽  
pp. 7343-7356 ◽  
Author(s):  
Mohammad Abdel-Halim ◽  
Adam B. Keeton ◽  
Evrim Gurpinar ◽  
Bernard D. Gary ◽  
Simon M. Vogel ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cells ◽  
Growth Inhibitors ◽  
Wild Type ◽  
Wild Type P53

Growth Suppression of Normal Mammary Epithelial Cells by Wild-Type p53

1993 ◽  
Vol 698 (1 Breast Cancer) ◽  
pp. 108-113 ◽  
Author(s):  
GIORGIO R. MERLO ◽  
TIZIANA VENESIO ◽  
DANIELA TAVERNA ◽  
ROBERT CALLAHAN ◽  
NANCY E. HYNES
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Growth Suppression ◽  
Mammary Epithelial ◽  
Wild Type ◽  
Wild Type P53 ◽  
Normal Mammary Epithelial
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