scholarly journals A High-Affinity Protein Binder that Blocks the IL-6/STAT3 Signaling Pathway Effectively Suppresses Non–Small Cell Lung Cancer

2014 ◽  
Vol 22 (7) ◽  
pp. 1254-1265 ◽  
Author(s):  
Joong-jae Lee ◽  
Hyun Jung Kim ◽  
Chul-Su Yang ◽  
Hyun-Ho Kyeong ◽  
Jung-Min Choi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
High Affinity ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals EPHA3 regulates the multidrug resistance of small cell lung cancer via the PI3K/BMX/STAT3 signaling pathway

Tumor Biology ◽  
2016 ◽  
Vol 37 (9) ◽  
pp. 11959-11971 ◽  
Author(s):  
Juan Peng ◽  
Qiongyao Wang ◽  
Huanxin Liu ◽  
Minting Ye ◽  
Xiaoxia Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Multidrug Resistance ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

IL-6 induces neuroendocrine dedifferentiation and cell proliferation in non-small cell lung cancer cells

2005 ◽  
Vol 289 (3) ◽  
pp. L446-L453 ◽  
Author(s):  
Kuo-Ting Chang ◽  
Chun-Ming Tsai ◽  
Yih-Chy Chiou ◽  
Chao-Hua Chiu ◽  
King-Song Jeng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell Lung Cancer ◽  
P38 Mapk ◽  
Cell Lung Cancer ◽  
Specific Inhibitor ◽  
Small Cell ◽  
Small Cell Lung ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Interleukin-6 (IL-6) has been identified as an important growth regulator of lung cancer cells. Elevation of serum levels of IL-6 has been found in a subpopulation of lung cancer patients, but rarely in patients with benign lung diseases. Approximately 15% of non-small cell lung cancer (NSCLC) tumors exhibit neuroendocrine (NE) properties (NSCLC-NE) and have been suggested to have the biological characteristics similar to small cell lung cancer (SCLC) with early metastasis and initial responsiveness to chemotherapy. We recently showed that IL-6 promotes cell proliferation and downregulates the expression of neuron-specific enolase (NSE, one of the major NE markers) in NSCLC-NE cells. In this study, we show that IL-6 stimulates a transient increase of tyrosine phosphorylation of STAT3 in a dose-dependent fashion. Inhibition of STAT3 signaling pathway by either AG-490 (JAK2-specific inhibitor) or overexpression of STAT3Y705F (a dominant-negative STAT3) reverses NSE expression in IL-6- treated NSCLC-NE cells. In addition, IL-6 induces phosphorylation and activation of p38 MAPK. SB-203580, a p38 MAPK-specific inhibitor, inhibits IL-6-induced p38 MAPK phosphorylating activity and suppresses IL-6-stimulated cell proliferation. Together, our results indicate that STAT3 signaling pathway is involved in IL-6-induced NE differentiation and that p38 MAPK is associated with IL-6-stimulated growth regulation in NSCLC-NE cells. These data suggest that both kinase pathways play critical roles in the pathogenesis of NSCLC-NE malignancies, providing new molecular targets for future therapeutic approaches.

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