scholarly journals Lactotransferrin: A candidate tumor suppressor-Deficient expression in human nasopharyngeal carcinoma and inhibition of NPC cell proliferation by modulating the mitogen-activated protein kinase pathway

2008 ◽  
Vol 123 (9) ◽  
pp. 2065-2072 ◽  
Author(s):  
Yanhong Zhou ◽  
Zhaoyang Zeng ◽  
Wenling Zhang ◽  
Wei Xiong ◽  
Minghua Wu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Suppressor ◽  
Mitogen Activated Protein Kinase ◽  
Candidate Tumor Suppressor ◽  
Human Nasopharyngeal Carcinoma ◽  
Mitogen Activated Protein ◽  
Kinase Pathway

scholarly journals Endothelin-1 Is a Potent Survival Factor for c-Myc-Dependent Apoptosis

1998 ◽  
Vol 12 (2) ◽  
pp. 172-180 ◽  
Author(s):  
Masayoshi Shichiri ◽  
John M. Sedivy ◽  
Fumiaki Marumo ◽  
Yukio Hirata
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Survival Function ◽  
Fibroblast Cell ◽  
Mitogen Activated Protein Kinase ◽  
Endothelin 1 ◽  
Survival Factor ◽  
Mitogen Activated Protein ◽  
Eta Receptor ◽  
Kinase Pathway

Abstract Many vertebrate cells are resistant to apoptotic stimuli, whose variety and the mechanisms involved are not fully understood. Endothelin-1 is an endothelium-derived vasoactive peptide that mediates many physiological functions, such as vasoconstriction and cell proliferation. Deregulated expression of c-Myc induces apoptosis in serum-deprived fibroblasts. Using a panel of isogenic fibroblast cell lines with differential c-myc expression levels, we demonstrate that low doses of endothelin-1 protect fibroblasts against serum deprivation-induced apoptosis, which occurs through a c-Myc-dependent process. The endothelin-1-induced cell survival was mediated by the ETA receptor and was not linked to the ability of endothelin-1 to induce cell proliferation. The survival function of endothelin-1 was abrogated by inhibiting the mitogen-activated protein kinase pathway. These results demonstrate a hitherto unappreciated role of endothelin-1 as a potent survival factor for c-Myc-dependent apoptosis, a process mediated by the ETA receptor and the mitogen-activated protein kinase pathway.

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