Wu Jing, Liu Shuye, Fan Zhijuan, Zhang Lei, Tian Yaqiong, Yang Rui
Department of Clinical Laboratory, Tianjin Third Central Hospital, No. 83 Jintang Road, Hedong District, Tianjin, 300170, China.
Research Center of Basic Medical Science, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin, 300070, China.
Tumour Biol. 2016 Jun;37(6):8391-401. doi: 10.1007/s13277-015-4744-9. Epub 2016 Jan 5.
Cell motility and chemotaxis play pivotal roles in the process of tumor development and metastasis. Protein kinase C ζ (PKC ζ) mediates epidermal growth factor (EGF)-stimulated chemotactic signaling pathway through regulating cytoskeleton rearrangement and cell adhesion. The purpose of this study was to develop anti-PKC ζ therapeutics for breast cancer metastasis. In this study, a novel and high-efficient PKC ζ inhibitor named PKCZI195.17 was screened out through a substrate-specific strategy. MTT assay was used to determine the cell viability of human breast cancer MDA-MB-231, MDA-MB-435, and MCF-7 cells while under PKCZI195.17 treatment. Wound-healing, chemotaxis, and Matrigel invasion assays were performed to detect the effects of PKCZI195.17 on breast cancer cells migration and invasion. Adhesion, actin polymerization, and Western blotting were performed to detect the effects of PKCZI195.17 on cells adhesion and actin polymerization, and explore the downsteam signaling mechanisms involved in PKC ζ inhibition. MDA-MB-231 xenograft was used to measure the in vivo anti-metastasis efficacy of PKCZI195.17. The compound PKCZI195.17 selectively inhibited PKC ζ kinase activity since it failed to inhibit PKC α, PKC β, PKC δ, PKC η, AKT2, as well as FGFR2 activity. PKCZI195.17 significantly impaired spontaneous migration, chemotaxis, and invasion of human breast cancer MDA-MB-231, MDA-MB-435, and MCF-7 cells, while PKCZI195.17 did not obviously inhibited cells viability. PKCZI195.17 also inhibited cells adhesion and actin polymerization through attenuating the phosphorylations of integrin β1, LIMK, and cofilin, which might be the downstream effectors of PKC ζ-mediated chemotaxis in MDA-MB-231 cells. Furthermore, PKCZI195.17 suppressed the breast cancer metastasis and increased the survival time of breast tumor-bearing mice. In summary, PKCZI195.17 was a PKC ζ-specific inhibitor which dampened cancer cell migration and metastasis and may serve as a novel therapeutic drug for breast cancer metastasis.
细胞运动性和趋化性在肿瘤发展和转移过程中起着关键作用。蛋白激酶Cζ(PKCζ)通过调节细胞骨架重排和细胞黏附来介导表皮生长因子(EGF)刺激的趋化信号通路。本研究的目的是开发用于乳腺癌转移的抗PKCζ治疗药物。在本研究中,通过一种底物特异性策略筛选出一种新型高效的PKCζ抑制剂,命名为PKCZI195.17。采用MTT法测定PKCZI195.17处理下人乳腺癌MDA-MB-231、MDA-MB-435和MCF-7细胞的活力。进行伤口愈合、趋化性和基质胶侵袭实验,以检测PKCZI195.17对乳腺癌细胞迁移和侵袭的影响。进行黏附、肌动蛋白聚合和蛋白质印迹实验,以检测PKCZI195.17对细胞黏附和肌动蛋白聚合的影响,并探索PKCζ抑制所涉及的下游信号机制。利用MDA-MB-231异种移植模型来测量PKCZI195.17的体内抗转移疗效。化合物PKCZI195.17选择性抑制PKCζ激酶活性,因为它未能抑制PKCα、PKCβ、PKCδ、PKCη、AKT2以及FGFR2的活性。PKCZI195.17显著损害人乳腺癌MDA-MB-231、MDA-MB-435和MCF-7细胞的自发迁移、趋化性和侵袭,而PKCZI195.17并未明显抑制细胞活力。PKCZI195.17还通过减弱整合素β1、LIMK和丝切蛋白的磷酸化来抑制细胞黏附和肌动蛋白聚合,这可能是PKCζ介导的MDA-MB-231细胞趋化的下游效应器。此外,PKCZI195.17抑制乳腺癌转移并延长荷瘤小鼠的存活时间。总之,PKCZI195.17是一种PKCζ特异性抑制剂,可抑制癌细胞迁移和转移,可能作为一种用于乳腺癌转移的新型治疗药物。