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Novel insights into breast cancer progression and metastasis: A multidisciplinary opportunity to transition from biology to clinical oncology.乳腺癌进展和转移的新见解：从生物学到临床肿瘤学的多学科转化机会。
Biochim Biophys Acta Rev Cancer. 2019 Aug;1872(1):138-148. doi: 10.1016/j.bbcan.2019.07.002. Epub 2019 Jul 23.
2
Bevacizumab in the neoadjuvant treatment of human epidermal growth factor receptor 2-negative breast cancer: A meta-analysis of randomized controlled trials.贝伐单抗在人表皮生长因子受体2阴性乳腺癌新辅助治疗中的应用：一项随机对照试验的荟萃分析
Mol Clin Oncol. 2019 Mar;10(3):357-365. doi: 10.3892/mco.2019.1796. Epub 2019 Jan 2.
3
Antileukemic activity and mechanism of action of the novel PI3K and histone deacetylase dual inhibitor CUDC-907 in acute myeloid leukemia.新型 PI3K 和组蛋白去乙酰化酶双重抑制剂 CUDC-907 在急性髓系白血病中的抗白血病活性及作用机制。
Haematologica. 2019 Nov;104(11):2225-2240. doi: 10.3324/haematol.2018.201343. Epub 2019 Feb 28.
4
Bortezomib sensitizes multiple myeloma to NK cells via ER-stress-induced suppression of HLA-E and upregulation of DR5.硼替佐米通过内质网应激诱导的HLA-E抑制和DR5上调使多发性骨髓瘤对自然杀伤细胞敏感。
Oncoimmunology. 2018 Nov 2;8(2):e1534664. doi: 10.1080/2162402X.2018.1534664. eCollection 2019.
5
MHY440, a Novel Topoisomerase Ι Inhibitor, Induces Cell Cycle Arrest and Apoptosis via a ROS-Dependent DNA Damage Signaling Pathway in AGS Human Gastric Cancer Cells.MHY440，一种新型拓扑异构酶 Ι 抑制剂，通过 ROS 依赖性 DNA 损伤信号通路诱导 AGS 人胃癌细胞的细胞周期停滞和凋亡。
Molecules. 2018 Dec 28;24(1):96. doi: 10.3390/molecules24010096.
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CUDC-907 blocks multiple pro-survival signals and abrogates microenvironment protection in CLL.CUDC-907 阻断多种存活信号并消除 CLL 微环境的保护作用。
J Cell Mol Med. 2019 Jan;23(1):340-348. doi: 10.1111/jcmm.13935. Epub 2018 Oct 24.
7
The next generation of PI3K-Akt-mTOR pathway inhibitors in breast cancer cohorts.乳腺癌队列中下一代 PI3K-Akt-mTOR 通路抑制剂。
Biochim Biophys Acta Rev Cancer. 2018 Dec;1870(2):185-197. doi: 10.1016/j.bbcan.2018.08.001. Epub 2018 Aug 21.
8
Efficiency of Cytokine-Induced Killer Cells in Combination with Chemotherapy for Triple-Negative Breast Cancer.细胞因子诱导的杀伤细胞联合化疗治疗三阴性乳腺癌的疗效
J Breast Cancer. 2018 Jun;21(2):150-157. doi: 10.4048/jbc.2018.21.2.150. Epub 2018 Jun 20.
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Phase 1/1b dose escalation and expansion study of BEZ235, a dual PI3K/mTOR inhibitor, in patients with advanced solid tumors including patients with advanced breast cancer.BEZ235（一种双重 PI3K/mTOR 抑制剂）在包括晚期乳腺癌患者在内的晚期实体瘤患者中的 1/1b 期剂量递增和扩展研究。
Cancer Chemother Pharmacol. 2018 Aug;82(2):285-298. doi: 10.1007/s00280-018-3610-z. Epub 2018 Jun 7.
10
Dual HDAC and PI3K Inhibition Abrogates NFκB- and FOXM1-Mediated DNA Damage Response to Radiosensitize Pediatric High-Grade Gliomas.双重 HDAC 和 PI3K 抑制消除 NFκB 和 FOXM1 介导的 DNA 损伤反应，增强儿童高级别脑胶质瘤的放射敏感性。
Cancer Res. 2018 Jul 15;78(14):4007-4021. doi: 10.1158/0008-5472.CAN-17-3691. Epub 2018 May 14.

CUDC-907通过上调乳腺癌细胞中DR5的表达来增强TRAIL诱导的细胞凋亡。

CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells.

作者信息

Li Zhao-Jun, Hou Ya-Jun, Hao Gang-Ping, Pan Xiao-Xuan, Fei Hong-Rong, Wang Feng-Ze

机构信息

School of Pharmacy, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian, 271000, People's Republic of China.

School of Life Sciences, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian, 271000, People's Republic of China.

出版信息

J Cell Commun Signal. 2020 Dec;14(4):377-387. doi: 10.1007/s12079-020-00558-3. Epub 2020 Mar 21.

DOI:10.1007/s12079-020-00558-3
PMID:32200503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7642015/
Abstract

CUDC-907 is a novel dual-acting inhibitor of phosphoinositide 3-kinase (PI3K) and histone deacetylase (HDAC). In this study, we aimed to explore the anticancer effects of CUDC-907 on human breast cancer cells. Our results showed that CUDC-907 effectively inhibited breast cancer cell proliferation. Flow cytometry analysis revealed that CUDC-907 induced cell cycle arrest and apoptosis in breast cancer cells. The combined treatment of CUDC-907 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resulted in a marked increase in apoptosis and cleavage of caspase-8, -9 and poly (ADP-ribose) polymerase (PARP) in breast cancer cells. CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL. Knockdown of DR5 abrogated apoptosis induced by the combination of CUDC-907 and TRAIL in breast cancer cells. CUDC-907 increased the phosphorylation of JNK and p38 MAPK. JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5. In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation. The combination of CUDC-907 and TRAIL may be a promising therapeutic approach in the treatment of breast cancer.

摘要

CUDC-907是一种新型的磷酸肌醇3-激酶（PI3K）和组蛋白去乙酰化酶（HDAC）双效抑制剂。在本研究中，我们旨在探究CUDC-907对人乳腺癌细胞的抗癌作用。我们的结果表明，CUDC-907能有效抑制乳腺癌细胞增殖。流式细胞术分析显示，CUDC-907可诱导乳腺癌细胞的细胞周期停滞和凋亡。CUDC-907与肿瘤坏死因子相关凋亡诱导配体（TRAIL）联合处理导致乳腺癌细胞凋亡显著增加，且半胱天冬酶-8、-9和聚（ADP-核糖）聚合酶（PARP）裂解。CUDC-907增强死亡受体5（DR5）的表达，降低抗凋亡分子XIAP、Bcl-2和Bcl-xL的水平。敲低DR5可消除CUDC-907与TRAIL联合诱导的乳腺癌细胞凋亡。CUDC-907增加JNK和p38丝裂原活化蛋白激酶（MAPK）的磷酸化。JNK抑制剂预处理减弱了CUDC-907诱导的DR5上调。总之，CUDC-907对乳腺癌细胞显示出强大的细胞毒性，并通过上调DR5促进TRAIL介导的凋亡。CUDC-907与TRAIL联合可能是治疗乳腺癌的一种有前景的治疗方法。