组蛋白脱乙酰基酶及其抑制剂对肿瘤的作用

国际肿瘤学杂志››2019,Vol. 46››Issue (4): 235-238.doi:10.3760/cma.j.issn.1673-422X.2019.04.009

组蛋白脱乙酰基酶及其抑制剂对肿瘤的作用

梁敬^1,3,韩莎²,姚静³,孔庆胜²

¹曲阜师范大学生命科学学院，济宁 273165；²山东省出生缺陷研究与转化协同创新中心，济宁 272067；³济宁医学院基础医学院，济宁 272067

收稿日期:2019-01-10修回日期:2019-02-28出版日期:2019-04-08发布日期:2019-05-29
通讯作者:孔庆胜，Email: jnyxykqs@163.com E-mail:jnyxykqs@163.com
基金资助:

国家自然科学基金（81603143）；山东省自然科学基金（ZR2013CM031）

Effect of histone deacetylase and its inhibitor on tumor

Liang Jing^1,3, Han Sha², Yao Jing³, Kong Qingsheng²

¹Faculty of Life Sciences, Qufu Normal University, Jining 273165, China;²Collaborative Innovation Center for Birth Defect Research and Transformation of Shandong Province, Jining 272067, China;³College of Basic Medical, Jining Medical University, Jining 272067, China

Received:2019-01-10Revised:2019-02-28Online:2019-04-08Published:2019-05-29
Contact:Kong Qingsheng, Email: jnyxykqs@163.com E-mail:jnyxykqs@163.com
Supported by:

National Natural Science Foundation of China (81603143); Natural Science Foundation of Shandong Province of China (ZR2013CM031)

摘要/Abstract

摘要：肿瘤的发生和进展是遗传和表观遗传共同作用的结果。组蛋白脱乙酰化修饰作为重要的表观遗传修饰的一种，对肿瘤的发生与发展有不可忽视的作用。组蛋白脱乙酰基酶在正常组织及细胞中的异常表达，会促进肿瘤的发展，并与肿瘤细胞的增殖和凋亡、血管生成、转移及耐药等方面相关，成为肿瘤治疗的新靶点。组蛋白脱乙酰基酶抑制剂作为抗肿瘤药物显示出良好的应用前景。

关键词:组蛋白脱乙酰基酶类,肿瘤转移,抗肿瘤药,组蛋白脱乙酰基酶抑制剂

Abstract:The occurrence and progress of tumor is the result of the interaction of heredity and epigenetics. Histone deacetylation modification, as an important epigenetic modification, plays an important role in tumorigenesis and development. The abnormal expression of histone deacetylase in normal tissues and cells promotes the development of tumor and is related to the proliferation and apoptosis, angiogenesis, metastasis and drug resistance of tumor cells, and becomes a new target of tumor therapy. Histone deacetylase inhibitors as antitumor drugs have a good prospect of application.

Key words:Histone deacetylases,Neoplasm metastasis,Antineoplastic agents,Histone deacetylase inhibitors

梁敬1,3,韩莎2,姚静3,孔庆胜2. 组蛋白脱乙酰基酶及其抑制剂对肿瘤的作用[J]. 国际肿瘤学杂志, 2019, 46(4): 235-238.

Liang Jing1,3, Han Sha2, Yao Jing3, Kong Qingsheng2. Effect of histone deacetylase and its inhibitor on tumor[J]. Journal of International Oncology, 2019, 46(4): 235-238.

参考文献

［1］ Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries［J］. CA Cancer J Clin, 2018, 68(6): 394-424. DOI: 10.3322/caac.21492. ［2］ La Noce M, Paino F, Mele L, et al. HDAC2 depletion promotes osteosarcoma′s stemness both in vitro and in vivo: a study on a putative new target for CSCs directed therapy［J］. J Exp Clin Cancer Res, 2018, 37(1): 296. DOI: 10.1186/s13046-018-0978-x. ［3］ Deng R, Zhang P, Liu W, et al. HDAC is indispensable for IFN-gamma-induced B7-H1 expression in gastric cancer［J］. Clin Epigenetics, 2018, 10(1): 153. DOI: 10.1186/s13148-018-0589-6. ［4］ Kang ZH, Wang CY, Zhang WL, et al. Histone deacetylase HDAC4 promotes gastric cancer SGC-7901 cells progression via p21 repression［J］. PLoS One, 2014, 9(6): e98894. DOI: 10.1371/journal.pone.0098894. ［5］ Dong J, Zheng N, Wang X, et al. A novel HDAC6 inhibitor exerts an anti-cancer effect by triggering cell cycle arrest and apoptosis in gastric cancer［J］. Eur J Pharmacol, 2018, 828: 67-79. DOI: 10.1016/j.ejphar.2018.03.026. ［6］ Ahn MY, Yoon JH. Histone deacetylase 7 silencing induces apoptosis and autophagy in salivary mucoepidermoid carcinoma cells［J］. J Oral Pathol Med, 2017, 46(4): 276-283. DOI: 10.1111/jop.12560. ［7］ Hung KC, Lin ML, Hsu SW, et al. Suppression of Akt-mediated HDAC3 expression and CDK2 T39 phosphorylation by a bichalcone analog contributes to S phase retardation of cancer cells［J］. Eur J Pharmacol, 2018, 829: 141-150. DOI: 10.1016/j.ejphar.2018.04.017. ［8］ Zhang H, Liu L, Liu C, et al. Notch3 overexpression enhances progression and chemoresistance of urothelial carcinoma［J］. Oncotarget, 2017, 8(21): 34362-34373. DOI: 10.18632/oncotarget.16156. ［9］ Pinazza M, Ghisi M, Minuzzo S, et al. Histone deacetylase 6 controls Notch3 trafficking and degradation in T-cell acute lymphoblastic leukemia cells［J］. Oncogene, 2018, 37(28): 3839-3851. DOI: 10.1038/s41388-018-0234-z. ［10］ Terranova-Barberio M, Thomas S, Ali N, et al. HDAC inhibition potentiates immunotherapy in triple negative breast cancer［J］. Oncotarget, 2017, 8(69): 114156-114172. DOI: 10.18632/oncotarget.23169. ［11］ Bian X, Liang Z, Feng A, et al. HDAC inhibitor suppresses proliferation and invasion of breast cancer cells through regulation of miR-200c targeting CRKL［J］. Biochem Pharmacol, 2018, 147: 30-37. DOI: 10.1016/j.bcp.2017.11.008. ［12］ Peng Z, Zhou W, Zhang C, et al. Curcumol controls choriocarcinoma stem-like cells self-renewal via repression of DNA methyltransferase (DNMT)- and histone deacetylase (HDAC)-mediated epigenetic regulation［J］. Med Sci Monit, 2018, 24: 461-472. ［13］ Gatla HR, Zou Y, Uddin MM, et al. Histone deacetylase (HDAC) inhibition induces IkappaB kinase (IKK)-dependent interleukin-8/CXCL8 expression in ovarian cancer cells［J］. J Biol Chem, 2017, 292(12): 5043-5054. DOI: 10.1074/jbc.M116.771014. ［14］ Kowshik J, Giri H, Kishore TK, et al. Ellagic acid inhibits VEGF/VEGFR2, PI3K/Akt and MAPK signaling cascades in the hamster cheek pouch carcinogenesis model［J］. Anticancer Agents Med Chem, 2014, 14(9): 1249-1260. ［15］ Huang YC, Huang FI, Mehndiratta S, et al. Anticancer activity of MPT0G157, a derivative of indolylbenzenesulfonamide, inhibits tumor growth and angiogenesis［J］. Oncotarget, 2015, 6(21): 18590-18601. DOI: 10.18632/oncotarget.4068. ［16］ Yao ZG, Li WH, Hua F, et al. LBH589 inhibits glioblastoma growth and angiogenesis through suppression of HIF-1alpha expression［J］. J Neuropathol Exp Neurol, 2017, 76(12): 1000-1007. DOI: 10.1093/jnen/nlx088. ［17］ Campbell S, Suwan K, Waramit S, et al. Selective inhibition of histone deacetylation in melanoma increases targeted gene delivery by a bacteriophage viral vector［J］. Cancers (Basel), 2018, 10(4). pii: cancers10040125. DOI: 10.3390/cancers10040125. ［18］ Tao H, Chen YY, Sun ZW, et al. Silence of HDAC6 suppressed esophageal squamous cell carcinoma proliferation and migration by disrupting chaperone function of HSP90［J］. J Cell Biochem, 2018, 119(8): 6623-6632. DOI: 10.1002/jcb.26841. ［19］ Wu YW, Hsu KC, Lee HY, et al. A novel dual HDAC6 and tubulin inhibitor, MPT0B451, displays anti-tumor ability in human cancer cells in vitro and in vivo［J］. Front Pharmacol, 2018, 9: 205. DOI: 10.3389/fphar.2018.00205. ［20］ Shen YF, Wei AM, Kou Q, et al. Histone deacetylase 4 increases progressive epithelial ovarian cancer cells via repression of p21 on fibrillar collagen matrices［J］. Oncol Rep, 2016, 35(2): 948-954. DOI: 10.3892/or.2015.4423. ［21］ Chen X, Li D, Gao Y, et al. Histone deacetylase SIRT6 inhibits glioma cell growth through down-regulating NOTCH3 expression［J］. Acta Biochim Biophys Sin (Shanghai), 2018, 50(4): 417-424. DOI: 10.1093/abbs/gmy019. ［22］ Liu C, Lv D, Li M, et al. Hypermethylation of miRNA-589 promoter leads to upregulation of HDAC5 which promotes malignancy in non-small cell lung cancer［J］. Int J Oncol, 2017, 50(6): 2079-2090. DOI: 10.3892/ijo.2017.3967. ［23］ Hegedus L, Padanyi R, Molnar J, et al. Histone deacetylase inhibitor treatment increases the expression of the plasma membrane Ca2+ pump PMCA4b and inhibits the migration of melanoma cells independent of ERK［J］. Front Oncol, 2017, 7: 95. DOI: 10.3389/fonc.2017.00095. ［24］ McLeod AB, Stice JP, Wardell SE, et al. Validation of histone deacetylase 3 as a therapeutic target in castration-resistant prostate cancer［J］. Prostate, 2018, 78(4): 266-277. DOI: 10.1002/pros.23467. ［25］ Luo S, Ma K, Zhu H, et al. Molecular, biological characterization and drug sensitivity of chidamide-resistant non-small cell lung cancer cells［J］. Oncol Lett, 2017, 14(6): 6869-6875. DOI: 10.3892/ol.2017.7060. ［26］ Wang Y, Jin T, Dai X, et al. Histone deacetylase enzyme silencing using shRNAs enhances radiosensitivity of SW579 thyroid cancer cells［J］. Mol Med Rep, 2016, 14(4): 3509-3516. DOI: 10.3892/mmr.2016.5711. ［27］ Yoon S, Eom GH. HDAC and HDAC inhibitor: from cancer to cardiovascular diseases［J］. Chonnam Med J, 2016, 52(1): 1-11. DOI: 10.4068/cmj.2016.52.1.1. ［28］ Bae J, Hideshima T, Tai YT, et al. Histone deacetylase (HDAC) inhibitor ACY241 enhances antitumor activities of antigen-specific central memory cytotoxic T lymphocytes against multiple myeloma and solid tumors［J］. Leukemia, 2018, 32(9): 1932-1947. DOI: 10.1038/s41375-018-0062-8. ［29］ Su Y, Hopfinger NR, Nguyen TD, et al. Epigenetic reprogramming of epithelial mesenchymal transition in triple negative breast cancer cells with DNA methyltransferase and histone deacetylase inhibitors［J］. J Exp Clin Cancer Res, 2018, 37(1): 314. DOI: 10.1186/s13046-018-0988-8. ［30］ Carbone C, Di Gennaro E, Piro G, et al. Tissue transglutaminase (TG2) is involved in the resistance of cancer cells to the histone deacetylase (HDAC) inhibitor vorinostat［J］. Amino Acids, 2017, 49(3): 517-528. DOI: 10.1007/s00726-016-2338-5.

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