國家衛生研究院 NHRI:Item 3990099045/9424
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    題名: Insulin-like growth factor-independent insulin-like growth factor binding protein 3 promotes cell migration and lymph node metastasis of oral squamous cell carcinoma cells by requirement of integrin beta1
    其他題名: Insulin-like growth factor-independent insulin-like growth factor binding protein 3 promotes cell migration and lymph node metastasis of oral squamous cell carcinoma cells by requirement of integrin β1
    作者: Yen, YC;Hsiao, JR;Jiang, SS;Chang, JS;Wang, SH;Shen, YY;Chen, CH;Chang, IS;Chang, JY;Chen, YW
    貢獻者: National Institute of Cancer Research;Pathology Core Laboratory;Division of Biostatistics and Bioinformatics
    摘要: Frequent metastasis to the cervical lymph nodes leads to poor survival of patients with oral squamous cell carcinoma (OSCC). To understand the underlying mechanisms of lymph node metastasis, two sublines were successfully isolated from cervical lymph nodes of nude mice through in vivo selection, and identified as originating from poorly metastatic parental cells. These two sublines specifically metastasized to cervical lymph nodes in 83% of mice, whereas OEC-M1 cells did not metastasize after injection into the oral cavity. After gene expression analysis, we identified insulin-like growth factor binding protein 3 (IGFBP3) as one of the significantly up-regulated genes in the sublines in comparison with their parental cells. Consistently, meta-analysis of the public microarray datasets and IGFBP3 immunohistochemical analysis revealed increased both levels of IGFBP3 mRNA and protein in human OSCC tissues when compared to normal oral or adjacent nontumorous tissues. Interestingly, the up-regulated IGFBP3 mRNA expression was significantly associated with OSCC patients with lymph node metastasis. IGFBP3 knockdown in the sublines impaired and ectopic IGFBP3 expression in the parental cells promoted migration, transendothelial migration and lymph node metastasis of orthotopic transplantation. Additionally, ectopic expression of IGFBP3 with an IGF-binding defect sustained the IGFBP3-enhanced biological functions. Results indicated that IGFBP3 regulates metastasis-related functions of OSCC cells through an IGF-independent mechanism. Furthermore, exogenous IGFBP3 was sufficient to induce cell motility and extracellular signal-regulated kinase (ERK) activation. The silencing of integrin beta1 was able to impair exogenous IGFBP3-mediated migration and ERK phosphorylation, suggesting a critical role of integrin beta1 in IGFBP3-enchanced functions.
    日期: 2015-12
    關聯: Oncotarget. 2015 Dec;6(39):41837-41855.
    Link to: http://dx.doi.org/10.18632/oncotarget.5995
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000366119600032
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84951761346
    顯示於類別:[江士昇] 期刊論文
    [張書銘] 期刊論文
    [陳雅雯] 期刊論文
    [張憶壽] 期刊論文
    [沈瑩瑩] 期刊論文

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