scholarly journals Shikonin causes cell-cycle arrest and induces apoptosis by regulating the EGFR–NF-κB signalling pathway in human epidermoid carcinoma A431 cells

2015 ◽  
Vol 35 (2) ◽  
Author(s):  
Rong Tian ◽  
You Li ◽  
Mei Gao
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Growth Factor Receptor ◽  
Signalling Pathways ◽  
Nuclear Factor ◽  
A431 Cells ◽  
Cycle Arrest ◽  
Epidermal Growth ◽  
Light Chain Enhancer ◽  
Human Epidermoid Carcinoma

Our findings indicated that shikonin-inhibited cell growth and caused cell-cycle arrest of the A431 cells through the regulation of apoptosis. Moreover, these effects were mediated, at least partially, by suppressing the activation of the EGFR (epidermal growth factor receptor)-NF-κB (nuclear factor kappa-light-chain-enhancer of activated B-cells) signalling pathways.

Abstract 1084: Honokiol induces G1phase cell cycle arrest in human epidermoid carcinoma A431 cells

2010 ◽  
Author(s):  
Ruth F. Guillermo ◽  
Shivani Chilampalli ◽  
Gudiseva Chandrasekhar ◽  
Radhey S. Kaushik ◽  
Hesham Fahmy ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Epidermoid Carcinoma ◽  
A431 Cells ◽  
Cycle Arrest ◽  
Human Epidermoid Carcinoma

scholarly journals Cell Density-Dependent Inhibition of Epidermal Growth Factor Receptor Signaling by p38α Mitogen-Activated Protein Kinase via Sprouty2 Downregulation

2009 ◽  
Vol 29 (12) ◽  
pp. 3332-3343 ◽  
Author(s):  
Aneta Swat ◽  
Ignacio Dolado ◽  
Jose Maria Rojas ◽  
Angel R. Nebreda
Keyword(s):  
Cell Cycle ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
Cell Cycle Arrest ◽  
Cell Density ◽  
Growth Factor Receptor ◽  
Cycle Arrest ◽  
Epidermal Growth

ABSTRACT Contact inhibition is a fundamental process in multicellular organisms aimed at inhibiting proliferation at high cellular densities through poorly characterized intracellular signals, despite availability of growth factors. We have previously identified the protein kinase p38α as a novel regulator of contact inhibition, as p38α is activated upon cell-cell contacts and p38α-deficient cells are impaired in both confluence-induced proliferation arrest and p27Kip1 accumulation. Here, we establish that p27Kip1 plays a key role downstream of p38α to arrest proliferation at high cellular densities. Surprisingly, p38α does not directly regulate p27Kip1 expression levels but leads indirectly to confluent upregulation of p27Kip1 and cell cycle arrest via the inhibition of mitogenic signals originating from the epidermal growth factor receptor (EGFR). Hence, confluent activation of p38α uncouples cell proliferation from mitogenic stimulation by inducing EGFR degradation through downregulation of the EGFR-stabilizing protein Sprouty2 (Spry2). Accordingly, confluent p38α-deficient cells fail to downregulate Spry2, providing them in turn with sustained EGFR signaling that facilitates cell overgrowth and oncogenic transformation. Our results provide novel mechanistic insight into the role of p38α as a sensor of cell density, which induces confluent cell cycle arrest via the Spry2-EGFR-p27Kip1 network.

EGF induces cell cycle arrest of A431 human epidermoid carcinoma cells

1986 ◽  
Vol 127 (1) ◽  
pp. 175-182 ◽  
Author(s):  
Carol L. MacLeod ◽  
Andrew Luk ◽  
Janice Castagnola ◽  
Maureen Cronin ◽  
John Mendelsohn
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Epidermoid Carcinoma ◽  
Cycle Arrest ◽  
Human Epidermoid Carcinoma
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