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一种新型组蛋白去乙酰化酶抑制剂MHY219通过HDAC1抑制人前列腺癌细胞的迁移。

A New Histone Deacetylase Inhibitor, MHY219, Inhibits the Migration of Human Prostate Cancer Cells via HDAC1.

作者信息

De Umasankar, Kundu Soma, Patra Nabanita, Ahn Mee Young, Ahn Ji Hae, Son Ji Yeon, Yoon Jung Hyun, Moon Hyung Ryoung, Lee Byung Mu, Kim Hyung Sik

机构信息

School of Pharmacy, Sungkyunkwan University, Suwon 440-746.

College of Pharmacy, Pusan National University, Busan 609-735.

出版信息

Biomol Ther (Seoul). 2015 Sep;23(5):434-41. doi: 10.4062/biomolther.2015.026. Epub 2015 Sep 1.

DOI:10.4062/biomolther.2015.026
PMID:26336583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4556203/
Abstract

Histone deacetylase (HDAC) inhibitors are considered novel agents for cancer chemotherapy. We previously investigated MHY219, a new HDAC inhibitor, and its potent anticancer activity in human prostate cancer cells. In the present study, we evaluated MHY219 molecular mechanisms involved in the regulation of prostate cancer cell migration. Similar to suberanilohydroxamic acid (SAHA), MHY219 inhibited HDAC1 enzyme activity in a dose-dependent manner. MHY219 cytotoxicity was higher in LNCaP (IC50=0.67 μM) than in DU145 cells (IC50=1.10 μM) and PC3 cells (IC50=5.60 μM) after 48 h of treatment. MHY219 significantly inhibited the HDAC1 protein levels in LNCaP and DU145 cells at high concentrations. However, inhibitory effects of MHY219 on HDAC proteins levels varied based on the cell type. MHY219 significantly inhibited LNCaP and DU145 cells migration by down-regulation of matrix metalloprotease-1 (MMP-1) and MMP-2 and induction of tissue inhibitor of metalloproteinases-1 (TIMP-1). These results suggest that MHY219 may potentially be used as an anticancer agent to block cancer cell migration through the repression of MMP-1 and MMP-2, which is related to the reduction of HDAC1.

摘要

组蛋白去乙酰化酶（HDAC）抑制剂被认为是癌症化疗的新型药物。我们之前研究了新型HDAC抑制剂MHY219及其在人前列腺癌细胞中的强大抗癌活性。在本研究中，我们评估了MHY219参与调节前列腺癌细胞迁移的分子机制。与辛二酰苯胺异羟肟酸（SAHA）类似，MHY219以剂量依赖性方式抑制HDAC1酶活性。处理48小时后，MHY219对LNCaP细胞（IC50 = 0.67μM）的细胞毒性高于DU145细胞（IC50 = 1.10μM）和PC3细胞（IC50 = 5.60μM）。高浓度时，MHY219显著抑制LNCaP和DU145细胞中的HDAC1蛋白水平。然而，MHY219对HDAC蛋白水平的抑制作用因细胞类型而异。MHY219通过下调基质金属蛋白酶-1（MMP-1）和MMP-2以及诱导金属蛋白酶组织抑制剂-1（TIMP-1），显著抑制LNCaP和DU145细胞迁移。这些结果表明，MHY219可能作为一种抗癌药物，通过抑制与HDAC1减少相关的MMP-1和MMP-2来阻断癌细胞迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/b1a4ae322670/bt-23-434f5a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/40caaa7070ac/bt-23-434f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/819dea4ecc57/bt-23-434f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/9dc49204fed6/bt-23-434f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/2015c3e75251/bt-23-434f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/b1a4ae322670/bt-23-434f5a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/40caaa7070ac/bt-23-434f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/819dea4ecc57/bt-23-434f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/9dc49204fed6/bt-23-434f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/2015c3e75251/bt-23-434f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e95c/4556203/b1a4ae322670/bt-23-434f5a.jpg

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