西达本胺抗肿瘤作用机制的研究进展
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摘要
西达本胺(Chidamide)是亚型选择性组蛋白脱乙酰酶(HDAC)的口服抑制剂,不仅能治疗癫痫,还具有较好的抗肿瘤活性。西达本胺可通过诱导细胞凋亡、分化、周期阻滞、抑制新血管生成及调控活性氧水平,从而发挥抗肿瘤活性。本文对近年来西达本胺的抗肿瘤活性及其作用机制进行综述。
Chidamide is an oral inhibitor of subtype selective histone deacetylase(HDAC), which can not only resist epilepsy, but also has good anti-tumor activity. It can exert anti-tumor activity by inducing cell apoptosis and differentiation, blocking cell cycle, inhibiting new angiogenesis and regulating the levels of ROS. This article will illustrate the antitumor pharmacological activity and mechanism of Chidamide.
Chidamide is an oral inhibitor of subtype selective histone deacetylase(HDAC), which can not only resist epilepsy, but also has good anti-tumor activity. It can exert anti-tumor activity by inducing cell apoptosis and differentiation, blocking cell cycle, inhibiting new angiogenesis and regulating the levels of ROS. This article will illustrate the antitumor pharmacological activity and mechanism of Chidamide.
引文
[1]食药讯.我国首批治疗外周T细胞淋巴瘤一类新药西达本胺片上市[N].首都食品与医药, 2015,(9):66.
[2]景赛赛,陈素梅,吴稚冰,等. HDACi抗肿瘤临床研究及机制进展[J].实用肿瘤杂志, 2016, 31(1):85-89.
[3]Chan TS, Tse E, Kwong YL. Chidamide in the treatment of peripheral T-cell lymphoma[J]. Onco Targets Ther, 2017,10:347-352. doi:10.2147/OTT. S93528.
[4]Pazin MJ, Kadonaga JT. What's up and down with histone deacetylation and transcription?[J]. Cell, 1997, 89(3):325-328.
[5]中国临床肿瘤学会(CSCO),中国抗淋巴瘤联盟(UCLI),中华医学会血液学分会(CSH)白血病淋巴瘤学组.西达本胺治疗外周T细胞淋巴瘤中国专家共识(2016版)[J].中国肿瘤临床, 2016, 43(8):317-323. doi:10.3969/j.issn.1000-8179.2016.08.239.
[6]曹利红,俞文娟,范翠华,等.西达本胺联合方案治疗急性髓系白血病二例[J].中华血液学杂志, 2017, 38(11):967-967. doi:10.3760/cma. j. issn.0253-2727.2017.11.013.
[7]尹子卉,吴仲闻,兰玉坤,等.新型抗肿瘤组蛋白去乙酰化酶抑制剂西达本胺的合成[J].中国新药杂志, 2004, 13(6):536-538. doi:10.3321/j. issn:1003-3734.2004.06.019.
[8]刘怀振,马居良,关承泰,等.一种西达本胺的合成方法:中国, CN201610476021. X[P].2016-06-27.
[9]赵建宏,户晖,关禹,等.西达本胺的工艺优化[J].中国医药工业杂志, 2017, 48(7):994-996. doi:10.16522/j.cnki. cjph.2017.07.006.
[10]王维,孟智启,石放雄.组蛋白修饰及其生物学效应[J].遗传, 2012, 34(7):810-818. doi:10.3724/SP.J.1005.2012.00810.
[11]刘春艳,孙海晶,陆军,等.组蛋白乙酰化与癌症[J].生物化学与生物物理进展, 2003, 30(1):19-23. doi:10.3321/j. issn:1000-3282.2003.01.004.
[12]汤屹,刘文励,周剑锋.组蛋白去乙酰化酶抑制剂治疗肿瘤的机制和临床应用研究进展[J].中华血液学杂志, 2002,23(6):329-331. doi:10.3760/j:issn:0253-2727.2002.06.015.
[13]Bassett SA, Barnett MP. The role of dietary histone deacetylases(HDACs)inhibitors in health and disease[J]. Nutrients, 2014, 6(10):4273-301. doi:10.3390/nu6104273.
[14]刘传. HDAC抑制联合DNA损伤药物增加化疗敏感性的机制研究[D].上海:第二军医大学, 2014.
[15]刘元江.组蛋白去乙酰化酶抑制剂的抗肿瘤活性[J].国外医学:药学分册, 2007,(1):70-71.
[16]张培培.西达本胺对不同增殖特性弥漫大B细胞淋巴瘤体外作用机制的研究[D].郑州:郑州大学, 2016.
[17]王志,张琦,林连兵,等.死亡受体5介导细胞凋亡的研究及应用[J].生物技术通报, 2011,(6):31-34.
[18]Zhao S, Guo J, Zhao Y, et al. Chidamide, a novel histone deacetylase inhibitor, inhibits the viability of MDS and AML cells by suppressing JAK2/STAT3 signaling[J]. Am J Transl Res, 2016, 8(7):3169-3178.
[19]胡璧,王建军,徐根兴.肿瘤坏死因子诱导凋亡配体(TRAIL)抗肿瘤治疗研究进展[J].药学与临床研究, 2008,16(3):194-200. doi:10.3969/j. issn.1673-7806.2008.03.010.
[20]付文锋,刘天礽.细胞周期抑制剂治疗肿瘤的进展[J].实用临床医学, 2015, 16(10):97-101. doi:10.13764/j.cnki. lcsy.2015.10.041.
[21]Zhou J, Zhang C, Sui X, et al. Histone deacetylase inhibitor chidamide induces growth inhibition and apoptosis in NK/T lymphoma cells through ATM-Chk2-p53-p21 signalling pathway[J]. Invest New Drugs, 2018, 36(4):571-580. doi:10.1007/s10637-017-0552-y.
[22]Liu Z, Ding K, Li L, et al. A novel histone deacetylase inhibitor Chidamide induces G0/G1 arrest and apoptosis in myelodysplastic syndromes[J]. Biomed Pharmacother,2016, 83:1032-1037. doi:10.1016/j. biopha.2016.08.023.
[23]Liu L, Qiu S, Liu Y, et al. Chidamide and 5-flurouracil show a synergistic antitumor effect on human colon cancer xenografts in nude mice[J]. Neoplasma, 2016, 63(2):193-200.doi:10.4149/203_150422N214.
[24]Gong K, Xie J, Yi H, et al. CS055(Chidamide/HBI-8000), a novel histone deacetylase inhibitor, induces G1 arrest, ROS-dependent apoptosis and differentiation in human leukaemia cells[J]. Biochem J, 2012, 443(3):735-746. doi:10.1042/BJ20111685.
[25]孙燕.肿瘤治疗的新里程碑——靶向药物治疗[J].肿瘤药学, 2011, 1(1):1-5. doi:10.3969/j. issn.2095-1264.2011.01.001.
[26]姜巩,魏凤梅,严小杰,等.分子靶向抗肿瘤药物的研究进展[J].肿瘤药学, 2016, 6(3):182-184. doi:10.3969/j.issn.2095-1264.2016.03.05.
[27]冯子侠,曹正洪.新型羟肟酸衍生物及其医疗应用:中国, CN103396417B[P].2015-02-19.
[28]Pourahmad J, Salimi A, Seydi E. Role of Oxygen Free Radicals in Cancer Development and Treatment[J]. Free Radic Dis.2016,(17):347-362.
[29]许艳,糜军.抗氧化剂在肿瘤防治中的应用及思考[J].肿瘤代谢与营养电子杂志, 2016, 3(3):139-143. doi:10.16689/j. cnki. cn11-9349/r.2016.03.003.
[30]Prasad S, Gupta SC, Tyagi AK. Reactive oxygen species(ROS)and cancer:Role of antioxidative nutraceuticals[J]. Cancer Lett, 2017, 387:95-105. doi:10.1016/j. canlet.2016.03.042.
[31]乔志新,贺敏,李伟静,等.西达本胺诱导胰腺癌细胞凋亡[J].生物技术通讯, 2013, 24(4):523-527. doi:10.3969/j.issn.1009-0002.2013.04.018.
[32]Zhang H, Li L, Li M, et al. Combination of betulinic acid and chidamide inhibits acute myeloid leukemia by suppression of the HIF1αpathway and generation of reactive oxygen species[J]. Oncotarget, 2017, 8(55):94743-94758. doi:10.18632/oncotarget.21889.
[33]Yu H, Zhang H, Chu Z, et al. Combination of betulinic acid and chidamide synergistically inhibits Epstein-Barr virus replication through over-generation of reactive oxygen species[J]. Oncotarget, 2017, 8(37):61646-61661. doi:10.18632/oncotarget.18661.
[2]景赛赛,陈素梅,吴稚冰,等. HDACi抗肿瘤临床研究及机制进展[J].实用肿瘤杂志, 2016, 31(1):85-89.
[3]Chan TS, Tse E, Kwong YL. Chidamide in the treatment of peripheral T-cell lymphoma[J]. Onco Targets Ther, 2017,10:347-352. doi:10.2147/OTT. S93528.
[4]Pazin MJ, Kadonaga JT. What's up and down with histone deacetylation and transcription?[J]. Cell, 1997, 89(3):325-328.
[5]中国临床肿瘤学会(CSCO),中国抗淋巴瘤联盟(UCLI),中华医学会血液学分会(CSH)白血病淋巴瘤学组.西达本胺治疗外周T细胞淋巴瘤中国专家共识(2016版)[J].中国肿瘤临床, 2016, 43(8):317-323. doi:10.3969/j.issn.1000-8179.2016.08.239.
[6]曹利红,俞文娟,范翠华,等.西达本胺联合方案治疗急性髓系白血病二例[J].中华血液学杂志, 2017, 38(11):967-967. doi:10.3760/cma. j. issn.0253-2727.2017.11.013.
[7]尹子卉,吴仲闻,兰玉坤,等.新型抗肿瘤组蛋白去乙酰化酶抑制剂西达本胺的合成[J].中国新药杂志, 2004, 13(6):536-538. doi:10.3321/j. issn:1003-3734.2004.06.019.
[8]刘怀振,马居良,关承泰,等.一种西达本胺的合成方法:中国, CN201610476021. X[P].2016-06-27.
[9]赵建宏,户晖,关禹,等.西达本胺的工艺优化[J].中国医药工业杂志, 2017, 48(7):994-996. doi:10.16522/j.cnki. cjph.2017.07.006.
[10]王维,孟智启,石放雄.组蛋白修饰及其生物学效应[J].遗传, 2012, 34(7):810-818. doi:10.3724/SP.J.1005.2012.00810.
[11]刘春艳,孙海晶,陆军,等.组蛋白乙酰化与癌症[J].生物化学与生物物理进展, 2003, 30(1):19-23. doi:10.3321/j. issn:1000-3282.2003.01.004.
[12]汤屹,刘文励,周剑锋.组蛋白去乙酰化酶抑制剂治疗肿瘤的机制和临床应用研究进展[J].中华血液学杂志, 2002,23(6):329-331. doi:10.3760/j:issn:0253-2727.2002.06.015.
[13]Bassett SA, Barnett MP. The role of dietary histone deacetylases(HDACs)inhibitors in health and disease[J]. Nutrients, 2014, 6(10):4273-301. doi:10.3390/nu6104273.
[14]刘传. HDAC抑制联合DNA损伤药物增加化疗敏感性的机制研究[D].上海:第二军医大学, 2014.
[15]刘元江.组蛋白去乙酰化酶抑制剂的抗肿瘤活性[J].国外医学:药学分册, 2007,(1):70-71.
[16]张培培.西达本胺对不同增殖特性弥漫大B细胞淋巴瘤体外作用机制的研究[D].郑州:郑州大学, 2016.
[17]王志,张琦,林连兵,等.死亡受体5介导细胞凋亡的研究及应用[J].生物技术通报, 2011,(6):31-34.
[18]Zhao S, Guo J, Zhao Y, et al. Chidamide, a novel histone deacetylase inhibitor, inhibits the viability of MDS and AML cells by suppressing JAK2/STAT3 signaling[J]. Am J Transl Res, 2016, 8(7):3169-3178.
[19]胡璧,王建军,徐根兴.肿瘤坏死因子诱导凋亡配体(TRAIL)抗肿瘤治疗研究进展[J].药学与临床研究, 2008,16(3):194-200. doi:10.3969/j. issn.1673-7806.2008.03.010.
[20]付文锋,刘天礽.细胞周期抑制剂治疗肿瘤的进展[J].实用临床医学, 2015, 16(10):97-101. doi:10.13764/j.cnki. lcsy.2015.10.041.
[21]Zhou J, Zhang C, Sui X, et al. Histone deacetylase inhibitor chidamide induces growth inhibition and apoptosis in NK/T lymphoma cells through ATM-Chk2-p53-p21 signalling pathway[J]. Invest New Drugs, 2018, 36(4):571-580. doi:10.1007/s10637-017-0552-y.
[22]Liu Z, Ding K, Li L, et al. A novel histone deacetylase inhibitor Chidamide induces G0/G1 arrest and apoptosis in myelodysplastic syndromes[J]. Biomed Pharmacother,2016, 83:1032-1037. doi:10.1016/j. biopha.2016.08.023.
[23]Liu L, Qiu S, Liu Y, et al. Chidamide and 5-flurouracil show a synergistic antitumor effect on human colon cancer xenografts in nude mice[J]. Neoplasma, 2016, 63(2):193-200.doi:10.4149/203_150422N214.
[24]Gong K, Xie J, Yi H, et al. CS055(Chidamide/HBI-8000), a novel histone deacetylase inhibitor, induces G1 arrest, ROS-dependent apoptosis and differentiation in human leukaemia cells[J]. Biochem J, 2012, 443(3):735-746. doi:10.1042/BJ20111685.
[25]孙燕.肿瘤治疗的新里程碑——靶向药物治疗[J].肿瘤药学, 2011, 1(1):1-5. doi:10.3969/j. issn.2095-1264.2011.01.001.
[26]姜巩,魏凤梅,严小杰,等.分子靶向抗肿瘤药物的研究进展[J].肿瘤药学, 2016, 6(3):182-184. doi:10.3969/j.issn.2095-1264.2016.03.05.
[27]冯子侠,曹正洪.新型羟肟酸衍生物及其医疗应用:中国, CN103396417B[P].2015-02-19.
[28]Pourahmad J, Salimi A, Seydi E. Role of Oxygen Free Radicals in Cancer Development and Treatment[J]. Free Radic Dis.2016,(17):347-362.
[29]许艳,糜军.抗氧化剂在肿瘤防治中的应用及思考[J].肿瘤代谢与营养电子杂志, 2016, 3(3):139-143. doi:10.16689/j. cnki. cn11-9349/r.2016.03.003.
[30]Prasad S, Gupta SC, Tyagi AK. Reactive oxygen species(ROS)and cancer:Role of antioxidative nutraceuticals[J]. Cancer Lett, 2017, 387:95-105. doi:10.1016/j. canlet.2016.03.042.
[31]乔志新,贺敏,李伟静,等.西达本胺诱导胰腺癌细胞凋亡[J].生物技术通讯, 2013, 24(4):523-527. doi:10.3969/j.issn.1009-0002.2013.04.018.
[32]Zhang H, Li L, Li M, et al. Combination of betulinic acid and chidamide inhibits acute myeloid leukemia by suppression of the HIF1αpathway and generation of reactive oxygen species[J]. Oncotarget, 2017, 8(55):94743-94758. doi:10.18632/oncotarget.21889.
[33]Yu H, Zhang H, Chu Z, et al. Combination of betulinic acid and chidamide synergistically inhibits Epstein-Barr virus replication through over-generation of reactive oxygen species[J]. Oncotarget, 2017, 8(37):61646-61661. doi:10.18632/oncotarget.18661.