Suppressor of cytokine signalling-2 limits igf1r-mediated regulation of epithelial-mesenchymal transition in lung adenocarcinoma
文献类型：期刊论文
| 作者 | Zhou, Yue1; Zhang, Zhilei2; Wang, Ning2; Chen, Jizheng3; Zhang, Xu2; Guo, Min4; Zhong, Li John2; Wang, Qian2 |
| 刊名 | Cell death & disease
 |
| 出版日期 | 2018-03-20 |
| 卷号 | 9页码:14 |
| ISSN号 | 2041-4889 |
| DOI | 10.1038/s41419-018-0457-5 |
| 通讯作者 | Wang, qian(wqian@njmu.edu.cn) |
| 英文摘要 | Non-small cell lung cancer (nsclc), including adenocarcinoma and squamous cell carcinoma, is the leading cause of death from lung malignancies and has a poor prognosis due to metastasis. suppressor of cytokine signalling-2 (socs2), a feedback inhibitor of cytokine signalling, has been shown to be involved in growth control. here, we show that socs2 were significantly downregulated in tumour foci in nsclc patients. the expression levels of socs2 significantly correlated with clinical stage, lymph node metastasis, histological subtype and survival time. in particular, the decreased expression of socs2 significantly associated with advanced pathological stage, lymph node metastasis and shorter overall survival in lung adenocarcinoma patients. in vivo animal results showed that overexpressed socs2 attenuated the metastatic characteristics of lung adenocarcinoma, including by inhibiting the epithelial-mesenchymal transition (emt). further functional studies indicated that insulin-like growth factor 1 (igf1)-driven migratory and invasive behaviours of lung adenocarcinoma cells can be partially suppressed by exogenous socs2 expression. investigations into the mechanism of action revealed that socs2 inhibits emt by inactivating signal transducer and activator of transcription 3 (stat3) and stat5 via the competitive binding of socs2 to the stat binding sites on igf1r. altogether, our results reveal an important role for socs2 dysregulation in the pathogenicity of lung adenocarcinoma, suggest its potential use as a biomarker for diagnosing lung adenocarcinoma, and paves the way to develop novel therapy targets as the axis of socs2-igf1r-stat in lung adenocarcinoma. |
| WOS关键词 | GROWTH-FACTOR RECEPTOR ; FACTOR-I RECEPTOR ; HUMAN HEPATOCELLULAR-CARCINOMA ; CHRONIC MYELOID-LEUKEMIA ; SOCS2 EXPRESSION ; STAT3 ACTIVATION ; JAK/STAT PATHWAY ; CELL-GROWTH ; CANCER ; INSULIN |
| WOS研究方向 | Cell Biology |
| WOS类目 | Cell Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000427908200002 |
| 出版者 | NATURE PUBLISHING GROUP |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2373334 |
| 专题 | 武汉病毒研究所 |
| 通讯作者 | Wang, Qian |
| 作者单位 | 1.Nanjing Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Nanjing 210029, Jiangsu, Peoples R China 2.Nanjing Med Univ, Dept Biochem & Mol Biol, Jiangsu Prov Key Lab Human Funct Genom, Nanjing 210029, Jiangsu, Peoples R China 3.Chinese Acad Sci, Wuhan Inst Virol, State Key Lab Virol, Wuhan 430071, Hubei, Peoples R China 4.China Pharmaceut Univ, Sch Life Sci & Technol, State Key Lab Nat Med, Nanjing 210009, Jiangsu, Peoples R China |
| 推荐引用方式 GB/T 7714 | Zhou, Yue,Zhang, Zhilei,Wang, Ning,et al. Suppressor of cytokine signalling-2 limits igf1r-mediated regulation of epithelial-mesenchymal transition in lung adenocarcinoma[J]. Cell death & disease,2018,9:14. |
| APA | Zhou, Yue.,Zhang, Zhilei.,Wang, Ning.,Chen, Jizheng.,Zhang, Xu.,...&Wang, Qian.(2018).Suppressor of cytokine signalling-2 limits igf1r-mediated regulation of epithelial-mesenchymal transition in lung adenocarcinoma.Cell death & disease,9,14. |
| MLA | Zhou, Yue,et al."Suppressor of cytokine signalling-2 limits igf1r-mediated regulation of epithelial-mesenchymal transition in lung adenocarcinoma".Cell death & disease 9(2018):14. |
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来源：武汉病毒研究所
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