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Mechanisms underlying the role of JNK signaling pathway in the invasion and metastasis of colon cancer cells

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Author:
No author available
Journal Title:
WORLD CHINESE JOURNAL OF DIGESTOLOGY
Issue:
21
DOI:
10.3969/j.issn.1009-3079.2009.21.005
Key Word:
大肠癌;侵袭;转移;c-Jun氨基末端激酶;纤维粘连蛋白

Abstract´╝Ü 目的:观察c-Jun氨基末端激酶(c-jun-N-terminal kinase,JNK)信号通路的活化对大肠癌细胞运动、侵袭的影响,并探讨大肠癌转移可能的分子机制.方法:LoVo细胞无血清饥饿24 h同步化后,对照组无纤维粘连蛋白(fibronectin,FN)干预,FN组给予FN 10,20,40 mg/L,24 h干预.JNK抑制剂组给予FN 40 mg/L+SP600125(20,40μmol/L)干预24 h.用Boyden小室法检测其体外运动和侵袭能力.Western blot法检测JNK磷酸化和MMP-9蛋白质表达.结果:FN可剂量性增加LoVo细胞运动和侵袭细胞数,SP600125能明显减少FN诱导的细胞运动和侵袭力.与对照组相比,FN 40 mg/L干预时P-JNK和MMP-9明显增高(38.39%±5.97% vs 28.61%±4.19%;58.25%±6.53% vs 33.43%±2.05%,均P<0.01).与FN 40 mg/L组相比,SP600125 40 μmol/L能明显抑制p-JNK和MMP-9蛋白的表达(29.59%±2.17% vs 38.39%±5.97%,36.69%±4.20% vs 58.25%±6.53%,均P<0.01).结论:大肠癌细胞JNK磷酸化可激活其下游成员使大肠癌基质金属蛋白酶的分泌增加,导致大肠癌细胞的运动和侵袭力增加,最终促进癌细胞的转移.

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