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De-N-乙酰GM3可通过尿激酶型纤溶酶原激活物受体信号传导依赖性MMP-2的活化促进黑色素瘤细胞的迁移和侵袭 |
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De-N-acetyl GM3 promotes melanoma cell migration and invasion through urokinase plasminogen activator receptor signaling-dependent MMP-2 activation |
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Liu J-W, Sun P, Yan Q, Paller AS, Gerami P, Ho N, Vashi N, Le Poole IC, Wang X-Q 2010/1/5 13:50:00 |
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Cancer Research, 2009, Volume 69, Issue 22
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We have recently discovered that de-N-acetyl GM3 [NeuNH2-LacCer, d-GM3], a derivative of ganglioside GM3, is specifically expressed in metastatic tumor cells and that its expression correlates with an enhanced metastatic phenotype. Although the classic N-acetylated form of GM3 (NeuAcLacCer, c-GM3) is found in both normal and tumor cells, metastatic tumor cells (but not other cells) predominantly express d-GM3 (82-95% of total GM3). d-GM3 expression is mainly found in metastatic melanomas, but not in benign nevi or the majority of primary melanomas. Using metastatic (d-GM3-positive) and poorly invasive (d-GM3-negative) human melanoma cell lines, we found that d-GM3 stimulates cell migration and invasion by increasing the expression and activation of urokinase-like plasminogen activator (uPA). Further studies showed that d-GM3 activates matrix metalloproteinase-2 (MMP-2), but not MMP-9, when uPA receptor signaling is activated. These results implicate d-GM3 as a specific marker for metastatic melanoma and a novel therapeutic target for neoplastic diseases. ©2009 American Association for Cancer Research.
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Correspondence Address: Wang, X.-Q.; Department of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States; email:x-wang1@northwestern.edu |
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疾病资源中心
王燕燕 王曙
上海交通大学附属瑞金医院内分泌科
患者,女,69岁。2009年1月无明显诱因下出现乏力,当时程度较轻,未予以重视。2009年3月患者乏力症状加重,尿色逐渐加深,大便习惯改变,颜色变淡。4月18日入我院感染科治疗,诉轻度头晕、心慌,体重减轻10kg。无肝区疼痛,无发热,无腹痛、腹泻、腹胀、里急后重,无恶性、呕吐等。入院半月前于外院就诊,查肝功能:ALT 601IU/L,AST 785IU/L,TBIL 97.7umol/L,白蛋白 41g/L,甲状腺功能:游离T3 30.6pmol/L,游离T4 51.9pmol/L,心电图示快速房颤。
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