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Cancer Cell:抑癌基因也可促肿瘤 对症下药很重要

2015-04-08 佚名 生物谷

近日,著名国际学术期刊cancer cell在线发表了德国科学家的一项最新研究进展,他们指出之前开发的TRAIL激动剂作为抗肿瘤药物在KRAS突变的癌症中不仅不能抑制肿瘤,反而会促进肿瘤发展,侵袭和转移,研究人员对其中的机制进行了深入研究。   许多癌症携带癌基因KRAS突变,之前对KRAS突变的癌症中介导癌症发展、侵袭和转移的效应因子一直没有得到全面了解。先前一些临床前和临床研究已

近日,著名国际学术期刊cancer cell在线发表了德国科学家的一项最新研究进展,他们指出之前开发的TRAIL激动剂作为抗肿瘤药物在KRAS突变的癌症中不仅不能抑制肿瘤,反而会促进肿瘤发展,侵袭和转移,研究人员对其中的机制进行了深入研究。
 
许多癌症携带癌基因KRAS突变,之前对KRAS突变的癌症中介导癌症发展、侵袭和转移的效应因子一直没有得到全面了解。先前一些临床前和临床研究已经证明TRAIL具有促细胞凋亡功能,但在开发TRAIL-R激动剂作为抗肿瘤药物的过程中发现许多肿瘤存在TRAIL-R的高表达,目前TRAIL-R在肿瘤中高表达的生物学功能一直没有得到很好的证明。
 
在该研究中,研究人员发现癌细胞内源性TRAIL-R信号通路在KRAS突变的癌症中能够驱动癌症进展、侵袭和转移,并对体内Rac-1激活有重要调节作用,这表明TRAIL/TRAIL-R系统的非凋亡相关功能在KRAS突变的癌症中得到了阳性选择。研究人员利用KRAS介导的非小细胞肺癌(NSCLC)和胰腺导管腺癌(PDAC)模型,在癌细胞内特异性敲除TRAIL-R,结果发现能够显著抑制肿瘤生长,阻断癌细胞转移,并通过抑制癌细胞自发性迁移、增殖和侵袭过程延长小鼠存活时间。与此一致的是,TRAIL-R的高水平表达与人类PDAC向淋巴管侵袭相关,也与携带KRAS突变的结肠癌病人恶性程度更高具有相关性。
 
研究人员指出,TRAIL/TRAIL-R系统可能在促进凋亡抵抗的癌症中发挥了重要作用,这也为许多类型的癌症中出现的TRAIL和TRAIL-R高表达提供了合理解释,因此,在此类癌症中抑制TRAIL/TRAIL-R,而非触发TRAIL/TRAIL-R系统,或许是一个有效的治疗策略。



原始出处:

Silvia von Karstedt, Annalisa Conti, Max Nobis, et al.Cancer Cell-Autonomous TRAIL-R Signaling Promotes KRAS-Driven Cancer Progression, Invasion, and Metastasis[J].Cancer Cell, April 2, 2015; DOI: http://dx.doi.org/10.1016/j.ccell.2015.02.014

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    2015-05-05 维他命
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