Molecular mechanism underlying the antiproliferative effect of suppressor of cytokine signaling-1 in non-small-cell lung cancer cells.
作者： Kazuki Shimada , Satoshi Serada , Minoru Fujimoto , Shintaro Nomura , Rie Nakatsuka
DOI: 10.1111/CAS.12266
关键词: Epidermal growth factor receptor 、 Cell growth 、 A549 cell 、 Biology 、 Signal transduction 、 Stat3 Signaling Pathway 、 Cancer research 、 Suppressor of cytokine signaling 1 、 Phosphorylation 、 Gene delivery
摘要: Lung cancer (LC) is the major cause of death by and number LC patients increasing worldwide. This study investigated therapeutic potential gene delivery using suppressor cytokine signaling 1 (SOCS-1), an endogenous inhibitor intracellular pathways, for treatment LC. To examine antitumor effect SOCS-1 overexpression on non-small-cell lung (NSCLC) cells, NSCLC cells (A549, LU65, PC9) were infected with adenovirus-expressing vector. The cell proliferation assay showed that A549 but not PC9, sensitive to gene-mediated suppression growth. Although JAK I could also inhibit LU65 appeared be more potent as suppress focal adhesion kinase epidermal growth factor receptor, well JAK/STAT3 pathway. Enhanced phosphorylation p53 protein was detected means phospho-kinase array in overexpressed compared control whereas no observed when used. Furthermore, adenoviral vector AdSOCS-1 vivo significantly suppressed a xenograft model. These results suggest effective therapy suppressing JAK/STAT, kinase, receptor pathways enhancing p53-mediated activity NSCLC.
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