科学家找到增加恶性乳腺癌对免疫治疗敏感性的分子开关

2016-08-31 佚名生物谷

科罗拉多大学癌症中心的研究人员在之前研究中发现实验药物AMPI-109能够有力杀灭三阴性乳腺癌细胞。但是培养皿中再有力的证据也不足以推动药物进入人类临床试验，即使是对三阴性乳腺癌这种致死率非常高并且目前仍然没有靶向治疗选择的疾病。现在一项发表在国际学术期刊Oncogenesis上的研究发现AMPI-109通过影响一种叫做PRL-3的分子发挥作用，抑制这种分子的活性可以让癌细胞进入“

科罗拉多大学癌症中心的研究人员在之前研究中发现实验药物AMPI-109能够有力杀灭三阴性乳腺癌细胞。但是培养皿中再有力的证据也不足以推动药物进入人类临床试验，即使是对三阴性乳腺癌这种致死率非常高并且目前仍然没有靶向治疗选择的疾病。

现在一项发表在国际学术期刊Oncogenesis上的研究发现AMPI-109通过影响一种叫做PRL-3的分子发挥作用，抑制这种分子的活性可以让癌细胞进入“睡眠”或衰老，随后导致细胞死亡。

研究人员表示：“我们已经知道有一条叫做TNF-R1的信号途径既可以帮助细胞存活也可以导致细胞死亡。但是导致该通路促进存活或促进死亡的信号是什么一直不清楚，特别是在癌细胞中。我们在三阴性乳腺癌细胞中观察到PRL-3可能是上述过程的一个调节因子。当这个基因发生激活，细胞就会存活，而当其活性受到抑制细胞就会衰老最终死亡。”

研究人员解释说，在环境较好的时候PRL-3能够启动一些基因的表达，招募免疫系统的一些成分促进癌症生长，而当环境比较恶劣的时候癌细胞就会进入睡眠。他们还在三阴性乳腺癌中敲低了PRL-3的表达，发现AMPI-109的作用效果与之非常类似，研究表明AMPI-109能够使细胞进入衰老，并且之后会让癌细胞度过这个阶段进入凋亡程序。

免疫治疗正逐渐成为多种癌症治疗的一线治疗选择。简单来说这种策略能够教会免疫系统识别并攻击肿瘤组织，但是一些癌症比较善于躲避免疫系统的攻击，因此许多免疫治疗方法都只能将癌症的发展维持在比较低的水平而无法完全清除。事实上一些免疫治疗方法也将癌症作为一种慢性疾病进行治疗，通过持续治疗无限期地遏制癌症发展。

这项研究提出，通过类似AMPI-109这样的药物抑制PRL-3活性可以向免疫系统发送信号对肿瘤进行定位，还可以增加肿瘤对免疫治疗的敏感性。如果未来研究结果仍然支持该研究结论，这种药物将成为借助免疫治疗方法靶向治疗三阴性乳腺癌的一种强力工具。

原始出处

H H Gari1, G D DeGala1, M S Lucia1 and J R Lambert.Loss of the oncogenic phosphatase PRL-3 promotes a TNF-R1 feedback loop that mediates triple-negative breast cancer growth.Oncogenesis.2016

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2016-09-26 1e10c84am36(暂无匿称)

文章很好值得关注

23 0
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2016-09-02 ms5236388012055669

#敏感性#

0 0
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2016-09-01 oo902

厉害的研究

25 0
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2016-09-01 医路开来

谢谢分享，，，，，

22 0
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2016-09-01 李东泽

很好，不错，以后会多学习

30 0

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