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含有MXXCW基序的肽通过一种新的作用机制抑制致癌性RET激酶活性。

Peptides containing the MXXCW motif inhibit oncogenic RET kinase activity with a novel mechanism of action.

作者信息

Takeda Kozue, Kawamoto Yoshiyuki, Nagasaki Yosuke, Okuno Yusuke, Goto Yuko, Iida Machiko, Yajima Ichiro, Ohgami Nobutaka, Kato Masashi

机构信息

College of Life and Health Sciences, Chubu University Kasugai, Aichi, Japan.

Medical Genomics Center, Nagoya University Hospital Nagoya, Japan.

出版信息

Am J Cancer Res. 2020 Jan 1;10(1):336-349. eCollection 2020.

Abstract

REarranged during Transition (RET) is a tyrosine kinase associated with the development of several malignancies. Identification of RET kinase inhibitors promises valuable therapeutic tools for the intervention of RET-driven tumors. Most currently available tyrosine kinase inhibitors target the ATP binding site, but there are several drawbacks of these ATP-competitive drugs. Therefore, there is a need to develop new kinase inhibitors with alternative mechanisms of action. We have previously reported that a conserved cysteine in the MXXCW motif of RET is crucial to the disulfide-bonded dimerization-linked activation of RET kinases. Reagents which bind to this cysteine may inhibit the activity of RET kinases through disulfide-bond mediated dimerization. Here, we examine the potential of MXXCW motif-containing peptides as candidate kinase inhibitors. We demonstrate that MXXCW motif-containing peptides bind to RET in a redox-sensitive manner and block enzymatic activity, causing inhibition of the RET-dependent activity of extracellular signal-regulated kinases and effectively reducing the malignant potential of RET-papillary thyroid carcinoma-1 (PTC)-expressing cells. These motif-containing peptides were also found to be effective against the drug resistant mutant of RET. The inhibition of RET kinase activity by these peptides resulted in suppression of RET-PTC-1-mediated cancer growth. The great potency of these cysteine targeted peptides could indicate promising approaches for novel molecular-targeted therapies for RET-associated cancers.

摘要

重排转位(RET)是一种与多种恶性肿瘤发生发展相关的酪氨酸激酶。鉴定RET激酶抑制剂有望为干预RET驱动的肿瘤提供有价值的治疗工具。目前大多数可用的酪氨酸激酶抑制剂靶向ATP结合位点,但这些ATP竞争性药物存在几个缺点。因此,需要开发具有替代作用机制的新型激酶抑制剂。我们之前报道过,RET的MXXCW基序中的一个保守半胱氨酸对于RET激酶的二硫键连接二聚化相关激活至关重要。与该半胱氨酸结合的试剂可能通过二硫键介导的二聚化抑制RET激酶的活性。在此,我们研究了含MXXCW基序的肽作为候选激酶抑制剂的潜力。我们证明含MXXCW基序的肽以氧化还原敏感的方式与RET结合并阻断酶活性,导致细胞外信号调节激酶的RET依赖性活性受到抑制,并有效降低表达RET-甲状腺乳头状癌-1(PTC)的细胞的恶性潜能。还发现这些含基序的肽对RET的耐药突变体有效。这些肽对RET激酶活性的抑制导致RET-PTC-1介导的癌症生长受到抑制。这些靶向半胱氨酸的肽的强大效力可能为RET相关癌症的新型分子靶向治疗指明了有前景的方法。

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