肺癌新疗法——EGFR靶向降解

2020-08-22 医药魔方 医药魔方

表皮生长因子受体(Epidermal growth factor receptor,EGFR)是控制上皮细胞生长和存活的关键因子,其高表达或异常激活与包括非小细胞肺癌(NSCLC)在内的多种癌症的肿瘤

表皮生长因子受体(Epidermal growth factor receptor,EGFR)是控制上皮细胞生长和存活的关键因子,其高表达或异常激活与包括非小细胞肺癌(NSCLC)在内的多种癌症的肿瘤进展和治疗耐药有关,因此,常被用于上皮恶性肿瘤的靶向治疗。

目前,所有可用的靶向EGFR的疗法,包括小分子酪氨酸激酶抑制剂(TKIs)和靶向EGFR的单克隆抗体,都集中于抑制EGFR激酶活性或诱导抗体和补体介导的细胞毒性作用。其中,EGFR抗体主要用于治疗晚期结直肠癌和头颈部肿瘤,因临床疗效有限,很少用于治疗NSCLC。而可逆或不可逆抑制EGFR酪氨酸激酶活性的第一代至第三代EGFR 酪氨酸激酶抑制剂(TKIs) 已被广泛应用于NSCLC的治疗,是这类癌症的一线疗法。

知识卡:EGFR是一种跨膜蛋白,由细胞外的配体结合区、疏水跨膜结构域和细胞内的激酶区3部分组成,其胞内结构包含1个酪氨酸激酶域和具有多个自身磷酸化位点的羧基末端尾,属于受体酪氨酸激酶家族。小分子EGFR酪氨酸激酶抑制剂的作用部位为胞内结构域。

被设计针对野生型EGFR (WT-EGFR)的吉非替尼和厄洛替尼是一代EGFR TKIs,但也对活性EGFR突变显示出了强大的选择性抑制作用。二代EGFR TKIs(如阿法替尼、达可替尼)被设计用于克服一代EGFR TKIs的获得性T790M耐药性,但由于毒性不可接受失败了。

新开发的三代EGFR TKIs(如奥希替尼和诺司替尼)与EGFR ATP结合位点上的半胱氨酸-797残基不可逆结合,相对于WT-EGFR,对携带激活的突变或T790M耐药突变的EGFR形式显示出优先的活性。

奥希替尼其实是一种EGFR/HER2双重抑制剂,可适度降低HER2的异常激活,而HER2异常激活是获得性抵抗EGFR TKIs的另一机制。尽管在临床应用中取得了成功,但也有研究报道了奥希替尼的获得性耐药,如C797S突变。

除了不可避免的获得性耐药,目前的EGFR TKIs对携带EGFR激活突变的患者更有效,而为大多数携带WT-EGFR的肺癌患者带来的益处有限。但越来越多的证据表明,WT-EGFR在肺癌的发病和进展中起着至关重要的作用。WT-EGFR表达升高不仅与三代EGFR TKIs的获得性耐药有关,而且还参与了突变KRAS活性的维持和KRAS驱动的NSCLC的发生。因此,迫切需要确定靶向治疗突变EGFR或WT-EGFR的替代作用机制。

越来越多的证据表明,EGFR的空间分布和稳定性也是调节肺癌进展的重要决定因素。在突变EGFR驱动的肺腺癌中,EGFR降解的失调会进一步加速肿瘤的发生和进展。这些发现强调了促进EGFR降解是靶向EGFR相关癌症的一种替代策略。

7月21日,发表在Nature Communications杂志上的一项研究中,由中国医学科学院药物研究所胡卓伟研究员和花芳研究员带领的团队发现,假性激酶Tribble 3 (TRIB3)表达升高与EGFR稳定性、循环、信号活性增强以及NSCLC进展呈正相关。TRIB3和EGFR同时高表达的肺癌患者生存率显着降低。

TRIB3作为一种压力传感器响应各种不同的压力源,通过与信号和功能蛋白相互作用参与慢性炎症、代谢和恶性疾病。最近有研究证实,TRIB3通过与自噬受体p62相互作用,削弱了自噬和蛋白酶体的降解功能,从而促进了多种癌症的发生和发展。TRIB3的缺失会导致各类癌症中多种肿瘤促进因子(包括EGFR)的表达显着下降。

在非小细胞肺癌中,TRIB3表达与EGFR呈正相关(来源:Nature Communications)

在这项新研究中,科学家们发现,TRIB3-EGFR相互作用导致EGFR的一系列翻译后修饰。TRIB3与EGFR相互作用,招募PKCα,在EGFR近膜区域(juxtamembrane region)诱导Thr654磷酸化以及WWP1诱导的Lys689泛素化,从而增强EGFR循环、稳定性和下游活性,以支持NSCLC的干性(stemness)。

TRIB3与EGFR相互作用,以促进PKCα介导的EGFR磷酸化(来源:NatureCommunications)

研究还证实,通过使用结合TRIB3的订书肽(stapled peptide)干扰TRIB3-EGFR的相互作用可加速EGFR降解,从而削弱NSCLC的进展,并使NSCLC细胞对化疗药物敏感。研究者们在多种肺癌体内外模型中证实了「靶向促进EGFR降解的先导订书肽」的抗肿瘤活性。

蛋白-蛋白相互作用可调节许多重要的生物过程,如细胞增殖、分化、程序性死亡等。这种相互作用也是许多疾病的治疗靶点,然而,一般情况下,由于蛋白-蛋白相互作用的界面太大,传统的小分子药物无法靶向这种界面,而蛋白质药物由于很难穿透细胞膜,也不能靶向细胞内的这种相互作用。订书肽是一类既能穿透细胞膜又能特异性靶向蛋白-蛋白相互作用的新分子类型,是一种具有α螺旋结构的新型多肽。相比天然多肽,订书肽具有更高的酶解稳定性,并可以进入细胞膜,因此具有更高的药理性能。

靶向EGFR稳定性可抑制肺癌的发生和发展(来源:Nature Communications)

这项新研究不仅发现了全新的抗肺癌靶点,更是在此基础上设计订书肽对靶点进行了概念验证。研究人员认为,这些发现表明,通过加速EGFR降解来干扰TRIB3-EGFR相互作用对治疗NSCLC具有的潜在效用,靶向促进EGFR降解而不是抑制其激酶活性是肺癌靶向治疗的新策略。

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    2021-04-11 Frank ong

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    2020-08-31 ms4000001617780766

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    2020-08-24 杀无敌战神

    学习

    0

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    2020-08-24 医者仁心
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    2020-08-24 kcb074
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    2020-08-23 ms7000000689223974

    很详细,很赞

    0

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    2020-08-23 红豆豆豆豆

    不错 点赞收藏学习起来

    0

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    2020-08-22 人家四月

    不错不错,学习了

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