@Article{096504015X14496932933610,
AUTHOR = {Fei Liu, Bihua Lin, Xin Liu, Wenzhang Zhang, Erying Zhang, Liang Hu, Yuefan Ma, Xiangyong Li, Xudong Tang},
TITLE = {ERK Signaling Pathway Is Involved in HPV-16 E6 but not E7 Oncoprotein-Induced HIF-1α Protein Accumulation in NSCLC Cells},
JOURNAL = {Oncology Research},
VOLUME = {23},
YEAR = {2015},
NUMBER = {3},
PAGES = {109--118},
URL = {http://www.techscience.com/or/v23n3/57559},
ISSN = {1555-3906},
ABSTRACT = {Extracellular signal-regulated kinase (ERK)1/2 signaling pathway plays a critical role in regulating tumor 
angiogenesis. Our previous studies have demonstrated that HPV-16 oncoproteins enhanced hypoxia-inducible 
factor-1α (HIF-1α) protein accumulation and vascular endothelial growth factor (VEGF) and interleukin-8 
(IL-8) expression in non-small cell lung cancer (NSCLC) cells, thus contributing to angiogenesis. In this 
study, we further investigated the role of ERK1/2 signaling pathway in HPV-16 oncoprotein-induced HIF-1α, 
VEGF, and IL-8 expression and in vitro angiogenesis in NSCLC cells. Our results showed that HPV-16 E6 and 
HPV-16 E7 oncoproteins promoted the activation of ERK1/2 signaling pathway in A549 and NCI-H460 cells. 
Moreover, PD98059, a specific inhibitor of ERK1/2, blocked in vitro angiogenesis stimulated by HPV-16 E6 
but not E7 oncoprotein. Additionally, HIF-1α protein accumulation and VEGF and IL-8 expression in NSCLC 
cells induced by HPV-16 E6 but not E7 oncoprotein were significantly inhibited by PD98059. Taken together, 
our results suggest that ERK1/2 signaling pathway is involved in HPV-16 E6 but not E7 oncoprotein-induced 
HIF-1α, VEGF, and IL-8 expression in NSCLC cells, leading to the enhanced angiogenesis in vitro.},
DOI = {10.3727/096504015X14496932933610}
}