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Int. J. Mol. Sci. 2017, 18(2), 258; doi:10.3390/ijms18020258

HDAC Inhibitors and RECK Modulate Endoplasmic Reticulum Stress in Tumor Cells

1
Department of Surgery, Far Eastern Memorial Hospital, 21, Sec. 2, Nan-Ya South Road, Banciao, Taipei 220, Taiwan
2
Department of Chemical Engineering and Materials Science, Yuan Ze University, 135 Yuan Tung Rd., Chung-Li, Taoyuan 320, Taiwan
3
Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, 7 Chung-Shan S. Rd., Taipei 100, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editor: Masato Matsuoka
Received: 29 December 2016 / Revised: 22 January 2017 / Accepted: 23 January 2017 / Published: 26 January 2017
(This article belongs to the Special Issue Modulators of Endoplasmic Reticulum Stress 2016)
View Full-Text   |   Download PDF [440 KB, uploaded 26 January 2017]   |  

Abstract

In the tumor microenvironment hypoxia and nutrient deprived states can induce endoplasmic reticulum (ER) stress. If ER stress is not relieved, the tumor cells may become apoptotic. Therefore, targeting ER homeostasis is a potential strategy for cancer treatment. Various chemotherapeutic agents including histone deacetylase (HDAC) inhibitors can induce ER stress to cause cell death in cancers. Some HDAC inhibitors can prevent HDAC from binding to the specificity protein 1-binding site of the promoter of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) and up-regulate RECK expression. Up-regulation of RECK expression by HDAC inhibitors has been observed in various cancer types. RECK is a tumor and metastasis suppressor gene and is critical for regulating tumor cell invasiveness and metastasis. RECK also modulates ER stress via binding to and sequestering glucose-regulated protein 78 protein, so that the transmembrane sensors, such as protein kinase RNA-like ER kinase are released to activate eukaryotic translational initiation factor 2α phosphorylation and enhance ER stress. Therefore, HDAC inhibitors may directly induce ER stress or indirectly induce this stress by up-regulating RECK in cancer cells. View Full-Text
Keywords: histone deacetylase inhibitors; reversion-inducing cysteine-rich protein with Kazal motifs; endoplasmic reticulum stress; cancers histone deacetylase inhibitors; reversion-inducing cysteine-rich protein with Kazal motifs; endoplasmic reticulum stress; cancers
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Chen, Y.; Tsai, Y.-H.; Tseng, S.-H. HDAC Inhibitors and RECK Modulate Endoplasmic Reticulum Stress in Tumor Cells. Int. J. Mol. Sci. 2017, 18, 258.

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