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一种用于治疗DNA错配修复缺陷肿瘤的新型化疗药物。

A Novel Chemotherapeutic Agent to Treat Tumors with DNA Mismatch Repair Deficiencies.

作者信息

Zhang Yongliang, Fox Jennifer T, Park Young-Un, Elliott Gene, Rai Ganesha, Cai Mengli, Sakamuru Srilatha, Huang Ruili, Xia Menghang, Lee Kyeryoung, Jeon Min Ho, Mathew Bijoy P, Park Hee Dong, Edelmann Winfried, Park Chan Young, Hong Sung You, Maloney David, Myung Kyungjae

机构信息

Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland.

Center for Genomic Integrity, Institute for Basic Science, Ulsan, Korea. Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Korea.

出版信息

Cancer Res. 2016 Jul 15;76(14):4183-91. doi: 10.1158/0008-5472.CAN-15-2974. Epub 2016 Jun 4.

Abstract

Impairing the division of cancer cells with genotoxic small molecules has been a primary goal to develop chemotherapeutic agents. However, DNA mismatch repair (MMR)-deficient cancer cells are resistant to most conventional chemotherapeutic agents. Here we have identified baicalein as a small molecule that selectively kills MutSα-deficient cancer cells. Baicalein binds preferentially to mismatched DNA and induces a DNA damage response in a MMR-dependent manner. In MutSα-proficient cells, baicalein binds to MutSα to dissociate CHK2 from MutSα leading to S-phase arrest and cell survival. In contrast, continued replication in the presence of baicalein in MutSα-deficient cells results in a high number of DNA double-strand breaks and ultimately leads to apoptosis. Consistently, baicalein specifically shrinks MutSα-deficient xenograft tumors and inhibits the growth of AOM-DSS-induced colon tumors in colon-specific MSH2 knockout mice. Collectively, baicalein offers the potential of an improved treatment option for patients with tumors with a DNA MMR deficiency. Cancer Res; 76(14); 4183-91. ©2016 AACR.

摘要

利用具有基因毒性的小分子来破坏癌细胞分裂一直是开发化疗药物的主要目标。然而,DNA错配修复(MMR)缺陷的癌细胞对大多数传统化疗药物具有抗性。在此,我们鉴定出黄芩素是一种能选择性杀死MutSα缺陷癌细胞的小分子。黄芩素优先结合错配的DNA,并以MMR依赖的方式诱导DNA损伤反应。在MutSα功能正常的细胞中,黄芩素与MutSα结合,使CHK2从MutSα上解离,导致S期停滞和细胞存活。相反,在MutSα缺陷细胞中,黄芩素存在时的持续复制会导致大量DNA双链断裂,最终导致细胞凋亡。一致的是,黄芩素能特异性地使MutSα缺陷的异种移植瘤缩小,并抑制结肠特异性MSH2基因敲除小鼠中AOM-DSS诱导的结肠肿瘤生长。总体而言,黄芩素为DNA MMR缺陷肿瘤患者提供了一种有改善潜力的治疗选择。《癌症研究》;76(14);4183 - 4191。©2016美国癌症研究协会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23b0/5033673/64e8d8e0de9d/nihms791641f1.jpg

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