https://scholars.lib.ntu.edu.tw/handle/123456789/476127
標題: | HDAC inhibitors and RECK modulate endoplasmic reticulum stress in tumor cells | 作者: | Chen Y. Tsai Y.-H. SHENG-HONG TSENG |
關鍵字: | Cancers; Endoplasmic reticulum stress; Histone deacetylase inhibitors; Reversion-inducing cysteine-rich protein with Kazal motifs | 公開日期: | 2017 | 出版社: | MDPI AG | 卷: | 18 | 期: | 2 | 來源出版物: | International Journal of Molecular Sciences | 摘要: | 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 2_ 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. ? 2017 by the authors; licensee MDPI, Basel, Switzerland. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85011101306&doi=10.3390%2fijms18020258&partnerID=40&md5=850953e25a8be68984a04b881f26995d https://scholars.lib.ntu.edu.tw/handle/123456789/476127 |
ISSN: | 1661-6596 | DOI: | 10.3390/ijms18020258 | SDG/關鍵字: | activating transcription factor 3; activating transcription factor 6; apicidin; caspase 4; caspase 7; epidermal growth factor receptor 2; gelatinase A; gelatinase B; glucose regulated protein 78; growth arrest and DNA damage inducible protein 153; histone deacetylase inhibitor; initiation factor 2alpha; messenger RNA; reactive oxygen metabolite; resveratrol; romidepsin; small interfering RNA; valproic acid; vorinostat; glycosylphosphatidylinositol anchored protein; histone deacetylase inhibitor; apoptosis; autophagy; bile duct carcinoma; breast cancer; cell invasion; cell proliferation; colon cancer; endoplasmic reticulum stress; fibrosarcoma; gene expression; glioma; human; ionizing radiation; multiple myeloma; nasopharynx carcinoma; non small cell lung cancer; osteosarcoma; reversion inducing cysteine rich protein with Kazal motif; Review; squamous cell carcinoma; translation initiation; tumor cell; tumor suppressor gene; unfolded protein response; upregulation; animal; biological model; cell death; drug effects; endoplasmic reticulum stress; metabolism; neoplasm; pathology; Animals; Cell Death; Endoplasmic Reticulum Stress; GPI-Linked Proteins; Histone Deacetylase Inhibitors; Humans; Models, Biological; Neoplasms |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。