國家衛生研究院 NHRI:Item 3990099045/4830
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/4830


    Title: ENO1, a potential prognostic head and neck cancer marker, promotes transformation partly via chemokine CCL20 induction
    Authors: Tsai, ST;Chien, IH;Shen, WH;Kuo, YZ;Jin, YT;Wong, TY;Hsiao, JR;Wang, HP;Shih, NY;Wu, LW
    Contributors: National Institute of Cancer Research
    Abstract: The success of using glycolytic inhibitors for cancer treatment depends on studying the individual role of frequently deregulated glycolytic genes in cancer. This report aims to study the prognostic implication, and determine the cellular role and action mechanism of glycolytic ENO1 overexpression in head and neck cancer. The relationship of ENO1 mRNA expression in 44-pair clinical specimens with patient clinicopathologic characteristics was analysed by semi-quantitative RT-PCR, Kaplan-Meier survival curve and Cox model analyses. Following ectopic ENO1 expression or knockdown, we studied the proliferative, migratory, invasive, colony-forming and tumourigenic abilities of ENO1-genetically altered cells. DNA microarray analysis was used to identify downstream targets responsible for the ENO1 action in the cells. The expression of ENO1 mRNA was increased in 68% of tumour (T) specimens when compared to their normal (N) counterparts, and positively associated with clinical progression (p < 0.05). High ENO1 expression (T/N ? 2) was frequently observed in the patients with large primary tumours, late clinical stages or advanced neck metastasis. Moreover, high ENO1 patients had significantly poorer clinical outcomes than low expressers (T/N < 2). Ectopic ENO1 expression stimulated cell transformation, invasion and tongue tumour formation. ENO1 knockdown abrogated the stimulation. Suppression of ENO1-induced proinflammatory CCL20 chemokine expression significantly attenuated its stimulatory effects on cell transformation and invasion. A concordant expression of ENO1 and CCL20 was validated both in ENO1-expresing cells and in clinical specimens. Together, we demonstrate a prognostic role of ENO1 overexpression in head and neck cancer and ENO1-mediated promotion of cell transformation and invasion partly via induced CCL20 expression.
    Date: 2010-06
    Relation: European Journal of Cancer. 2010 Jun;46(9):1712-1723.
    Link to: http://dx.doi.org/10.1016/j.ejca.2010.03.018
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0959-8049&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000279387700034
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77952584341
    Appears in Collections:[Neng-Yao Shih] Periodical Articles

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