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Article ; Online: A dual inhibitor targeting HMG-CoA reductase and histone deacetylase mitigates neurite degeneration in

Lin, Chin-Hsien / Lin, Han-Yi / Fang, Jim-Min / Chen, Ching-Chow

Aging

2020 Volume 12, Issue 24, Page(s) 25581–25598

Abstract: Parkinson's disease (PD) is among the most common neurodegenerative disorders, and its etiology involves both genetic and environmental factors. The leucine-rich repeat kinase (LRRK2) G2019S mutation is the most common genetic cause of familial and ... ...

Abstract	Parkinson's disease (PD) is among the most common neurodegenerative disorders, and its etiology involves both genetic and environmental factors. The leucine-rich repeat kinase (LRRK2) G2019S mutation is the most common genetic cause of familial and sporadic PD. Current treatment is limited to dopaminergic supplementation, as no disease-modifying therapy is available yet. Recent evidence reveals that HMG-CoA reductase (HMGR) inhibitors (statins) exert neuroprotection through anti-neuroinflammatory effects, and histone deacetylase (HDAC) inhibitors mitigate neurodegeneration by promoting the transcription of neuronal survival factors. We designed and synthesized a dual inhibitor, statin hydroxamate JMF3086, that simultaneously inhibits HMGR and HDAC, and examined its neuroprotective effects on
MeSH term(s)	Animals ; Drosophila ; Hippocampus/drug effects ; Hippocampus/metabolism ; Hippocampus/pathology ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Mice ; Mice, Transgenic ; Nerve Degeneration/drug therapy ; Nerve Degeneration/metabolism ; Nerve Degeneration/pathology ; Neurites/drug effects ; Neurites/metabolism ; Neurites/pathology ; Neuronal Outgrowth/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Parkinsonian Disorders/drug therapy ; Parkinsonian Disorders/genetics ; Parkinsonian Disorders/metabolism ; Parkinsonian Disorders/pathology ; Phosphorylation/drug effects
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Neuroprotective Agents ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2020-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.104165
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Article: Neuroinflammation Upregulated Neuronal Toll-Like Receptors 2 and 4 to Drive Synucleinopathy in Neurodegeneration.

Chung, Lucia Yi-Ru / Lin, Yi-Ting / Liu, Chi / Tai, Yi-Cheng / Lin, Han-Yi / Lin, Chin-Hsien / Chen, Ching-Chow

Frontiers in pharmacology

2022 Volume 13, Page(s) 845930

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2022-03-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.845930
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Article ; Online: Signal transduction pathways of inflammatory gene expressions and therapeutic implications.

Chen, Ching-Chow

Current pharmaceutical design

2006 Volume 12, Issue 27, Page(s) 3497–3508

Abstract: Intercellular adhesion molecule-1 (ICAM-1), an inducible cell adhesion glycoprotein of the immunoglobulin supergene family and cyclooxygenase-2 (COX-2), an inducible prostaglandin G/H synthase, are overexpressed by proinflammatory mediators in a wide ... ...

Abstract	Intercellular adhesion molecule-1 (ICAM-1), an inducible cell adhesion glycoprotein of the immunoglobulin supergene family and cyclooxygenase-2 (COX-2), an inducible prostaglandin G/H synthase, are overexpressed by proinflammatory mediators in a wide variety of cell types. These stimuli increase ICAM-1 or COX-2 expression primarily through activation of ICAM-1 or COX-2 gene transcription. The architecture of the ICAM-1 or COX-2 promoter is complex, containing a large number of binding site for inducible transcription factors, the most important of which is NF-kB. NF-kB acts in concert with other transcription factors or transcriptional coactivators which facilitate the assembly of distinct stereospecific transcription complexes on the ICAM-1 or COX-2 promoter. These transcription complexes presumably mediate the induction of ICAM-1 or COX-2 expression in different cell types and in response to different stimuli. In this review, I summarize the current understanding of ICAM-1 and COX-2 gene regulation with a particular emphasis on the transcription factors or coactivators, and signal transduction pathways critical for their expression. A PKC-dependent c-Src pathway activating NF-kB or GAS to enhance ICAM-1 or COX-2 gene expression is discussed. Furthermore, natural products and novel agents targeting on the transcription factor with potential anti-inflammation and anti-tumor activity are also discussed.
MeSH term(s)	Animals ; Base Sequence ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Molecular Sequence Data ; Signal Transduction/drug effects ; Signal Transduction/genetics
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2006-01-23
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161206778343028
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Zs.A 4714: Show issues

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Article ; Online: Life or death? Autophagy in anticancer therapies with statins and histone deacetylase inhibitors.

Yang, Pei-Ming / Chen, Ching-Chow

Autophagy

2011 Volume 7, Issue 1, Page(s) 107–108

Abstract: Autophagy, which could be either cytoprotective or cytotoxic, is often observed in tumor cells in response to chemotherapy. Understanding the signaling pathways involved in the regulation of autophagy represents a new direction in the development of ... ...

Abstract	Autophagy, which could be either cytoprotective or cytotoxic, is often observed in tumor cells in response to chemotherapy. Understanding the signaling pathways involved in the regulation of autophagy represents a new direction in the development of anticancer therapies. Our recent studies investigate the role of autophagy in the anticancer effects of statins and histone deacetylase: inhibitors (HDACi). Inhibition of autophagy enhances the efficacy of statins, whereas autophagic cell death in cancer cells is induced by HDACi. Here, we will discuss the differential signaling pathways elicited by statins and HDACi. We find that AMPK, cytoplasmic p21 and Akt signaling are crucial determinants of cell fates (i.e., life or death) while autophagy is induced.
MeSH term(s)	Adenylate Kinase/metabolism ; Antineoplastic Agents/therapeutic use ; Autophagy/drug effects ; Cell Survival/drug effects ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Enzyme Activation/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylase Inhibitors/therapeutic use ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Models, Biological ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	Antineoplastic Agents ; Cyclin-Dependent Kinase Inhibitor p21 ; Histone Deacetylase Inhibitors ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2011-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.7.1.13988
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Zs.A 6741: Show issues

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Article ; Online: Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress.

Lin, Yu-Chin / Wu, Meng-Hsuan / Wei, Tzu-Tang / Lin, Yun-Chieh / Huang, Wen-Chih / Huang, Liang-Yu / Lin, Yi-Ting / Chen, Ching-Chow

Oncotarget

2019 Volume 10, Issue 37, Page(s) 3577–3578

Abstract: This corrects the article DOI: 10.18632/oncotarget.1628.]. ...

Abstract	[This corrects the article DOI: 10.18632/oncotarget.1628.].
Language	English
Publishing date	2019-05-28
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26997
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Article ; Online: Correction: Metformin sensitizes anticancer effect of dasatinib in head and neck squamous cell carcinoma cells through AMPK-dependent ER stress.

Lin, Yu-Chin / Wu, Meng-Hsuan / Wei, Tzu-Tang / Lin, Yun-Chieh / Huang, Wen-Chih / Huang, Liang-Yu / Lin, Yi-Ting / Chen, Ching-Chow

Oncotarget

2019 Volume 10, Issue 55, Page(s) 5724–5725

Abstract: This corrects the article DOI: 10.18632/oncotarget.1628.]. ...

Abstract	[This corrects the article DOI: 10.18632/oncotarget.1628.].
Language	English
Publishing date	2019-10-01
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27228
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Article ; Online: Metabolic targeting of HIF-1α potentiates the therapeutic efficacy of oxaliplatin in colorectal cancer.

Wei, Tzu-Tang / Lin, Yi-Ting / Tang, Shao-Pu / Luo, Cong-Kai / Tsai, Chiou-Tsun / Shun, Chia-Tung / Chen, Ching-Chow

Oncogene

2019 Volume 39, Issue 2, Page(s) 414–427

Abstract: Drug resistance is a major problem limiting the efficacy of chemotherapy in cancer treatment, and the hypoxia-induced stabilization of HIF-1α plays a role in this process. HIF-1α overexpression has been observed in a variety of human cancers, including ... ...

Abstract	Drug resistance is a major problem limiting the efficacy of chemotherapy in cancer treatment, and the hypoxia-induced stabilization of HIF-1α plays a role in this process. HIF-1α overexpression has been observed in a variety of human cancers, including colorectal cancer (CRC). Therefore, targeting HIF-1α is a promising strategy for overcoming chemoresistance to enhance the efficacy of chemotherapies in CRC. Here, we show that DNMT inhibitors can induce HIF-1α degradation to overcome oxaliplatin resistance and enhance anti-CRC therapy. We found that a low-toxicity DNMT inhibitor, zebularine, could downregulate HIF-1α expression and overcome hypoxia-induced oxaliplatin resistance in HCT116 cells and showed efficacy in HCT116 xenograft models and AOM/DSS-induced CRC mouse models. Zebularine could induce the degradation of HIF-1α protein through hydroxylation. LC-MS analysis showed a decrease in succinate in various CRC cells under hypoxia and in colon tissues of AOM/DSS-induced CRC mice. The decrease was reversed by zebularine. Tumor angiogenesis was also reduced by zebularine. Furthermore, zebularine potentiated the anticancer effect of oxaliplatin in AOM/DSS-induced CRC models. This finding provides a new strategy in which an increase in HIF-1α hydroxylation could overcome oxaliplatin resistance to enhance anti-CRC therapy.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Colorectal Neoplasms/blood supply ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Cytidine/analogs & derivatives ; Cytidine/pharmacology ; Down-Regulation/drug effects ; Drug Resistance, Neoplasm/drug effects ; Drug Synergism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; HCT116 Cells ; Humans ; Hydroxylation/drug effects ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice ; Molecular Targeted Therapy ; Neovascularization, Pathologic/drug therapy ; Oxaliplatin/pharmacology ; Oxaliplatin/therapeutic use ; Protein Stability/drug effects ; Proteolysis/drug effects ; Vascular Endothelial Growth Factor A/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Vascular Endothelial Growth Factor A ; Oxaliplatin (04ZR38536J) ; Cytidine (5CSZ8459RP) ; pyrimidin-2-one beta-ribofuranoside (7A9Y5SX0GY)
Language	English
Publishing date	2019-09-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-019-0999-8
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Zs.A 2218: Show issues

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Article: HDAC inhibition upregulates the expression of angiostatic ADAMTS1.

Chou, Chia-Wei / Chen, Ching-Chow

FEBS letters

2008 Volume 582, Issue 29, Page(s) 4059–4065

Abstract: HDAC inhibitors are promising anticancer agents that induce cell cycle arrest and apoptosis. However, the role of HDACs in cancer progression, such as angiogenesis and metastasis, remains largely unexplored. Among various HDAC inhibitors, we demonstrate ... ...

Abstract	HDAC inhibitors are promising anticancer agents that induce cell cycle arrest and apoptosis. However, the role of HDACs in cancer progression, such as angiogenesis and metastasis, remains largely unexplored. Among various HDAC inhibitors, we demonstrate that TSA and SAHA upregulated the expression of angiostatic ADAMTS1 in A549 cells. HDAC6 inhibitor tubacin, and knockdown of HDAC6, also lead to ADAMTS1 upregulation. By reporter, DAPA, and ChIP assays, the proximal GC boxes were demonstrated to be essential for ADAMTS1 induction. Decreased binding of SP1 and HDAC6 to the ADAMTS1 promoter after TSA treatment was also seen. These data suggest the involvement of HDAC6 and SP1 in the HDACi-induced expression of angiostatic ADAMTS1.
MeSH term(s)	ADAM Proteins/biosynthesis ; ADAM Proteins/genetics ; ADAMTS1 Protein ; Angiostatic Proteins/biosynthesis ; Angiostatic Proteins/genetics ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Enzyme Inhibitors/pharmacology ; Histone Deacetylase 6 ; Histone Deacetylase Inhibitors ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Promoter Regions, Genetic ; Sp1 Transcription Factor/metabolism ; Up-Regulation
Chemical Substances	Angiostatic Proteins ; Antineoplastic Agents ; Enzyme Inhibitors ; Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Sp1 Transcription Factor ; trichostatin A (3X2S926L3Z) ; vorinostat (58IFB293JI) ; ADAM Proteins (EC 3.4.24.-) ; ADAMTS1 Protein (EC 3.4.24.-) ; ADAMTS1 protein, human (EC 3.4.24.-) ; HDAC6 protein, human (EC 3.5.1.98) ; Histone Deacetylase 6 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2008-12-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2008.10.048
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Article ; Online: CD1d induction in solid tumor cells by histone deacetylase inhibitors through inhibition of HDAC1/2 and activation of Sp1.

Yang, Pei-Ming / Lin, Pei-Jie / Chen, Ching-Chow

Epigenetics

2012 Volume 7, Issue 4, Page(s) 390–399

Abstract: CD1d is a MHC class-like molecule that presents glycolipids to natural killer T (NKT) cells, then regulates innate and adaptive immunity. The regulation of CD1d gene expression in solid tumors is still largely unknown. Gene expression can be ... ...

Abstract	CD1d is a MHC class-like molecule that presents glycolipids to natural killer T (NKT) cells, then regulates innate and adaptive immunity. The regulation of CD1d gene expression in solid tumors is still largely unknown. Gene expression can be epigenetically regulated by DNA methylation and histone acetylation. We found that histone deacetylase inhibitors, trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), induced CD1d gene expression in human (A549 and NCI-H292) and mouse (TC-1 and B16/F0) cancer cells. Simultaneous knockdown of HDAC1 and 2 induced CD1d gene expression. Sp1 inhibitor mitramycin A (MTM) blocked TSA- and SAHA-induced CD1d mRNA expression and Sp1 luciferase activity. Co-transfection of GAL4-Sp1 and Fc-luciferase reporters demonstrated that TSA and SAHA induced Sp1 luciferase reporter activity by enhancing Sp1 transactivation activity. The binding of Sp1 to CD1d promoter and histone H3 acetylation on Sp1 sites were increased by TSA and SAHA. These results indicate that TSA and SAHA could up-regulate CD1d expression in tumor cells through inhibition of HDAC1/2 and activation of Sp1.
MeSH term(s)	Acetylation ; Animals ; Antigens, CD1d/genetics ; Antigens, CD1d/metabolism ; Base Sequence ; Binding Sites ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Enzyme Activation ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Genes, Reporter ; Histone Deacetylase 1/genetics ; Histone Deacetylase 1/metabolism ; Histone Deacetylase 2/genetics ; Histone Deacetylase 2/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Histones/genetics ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Luciferases/genetics ; Luciferases/metabolism ; Mice ; Molecular Sequence Data ; Plicamycin/pharmacology ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Sp1 Transcription Factor/genetics ; Sp1 Transcription Factor/metabolism ; Transcriptional Activation ; Transfection ; Vorinostat
Chemical Substances	Antigens, CD1d ; CD1D protein, human ; Cd1d1 protein, mouse ; Histone Deacetylase Inhibitors ; Histones ; Hydroxamic Acids ; RNA, Messenger ; RNA, Small Interfering ; Sp1 Transcription Factor ; trichostatin A (3X2S926L3Z) ; Vorinostat (58IFB293JI) ; Luciferases (EC 1.13.12.-) ; HDAC1 protein, human (EC 3.5.1.98) ; HDAC2 protein, human (EC 3.5.1.98) ; Hdac1 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Histone Deacetylase 2 (EC 3.5.1.98) ; Plicamycin (NIJ123W41V)
Language	English
Publishing date	2012-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.4161/epi.19373
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Article: Akt phosphorylation of p300 at Ser-1834 is essential for its histone acetyltransferase and transcriptional activity.

Huang, Wei-Chien / Chen, Ching-Chow

Molecular and cellular biology

2005 Volume 25, Issue 15, Page(s) 6592–6602

Abstract: The PI3K/Akt pathway plays a critical role in the regulation of gene expression induced by numerous stimuli. p300, a transcriptional coactivator, acts in concert with transcription factors to facilitate gene expression. Here, we show that Akt is ... ...

Abstract	The PI3K/Akt pathway plays a critical role in the regulation of gene expression induced by numerous stimuli. p300, a transcriptional coactivator, acts in concert with transcription factors to facilitate gene expression. Here, we show that Akt is activated and translocated to the nucleus in response to tumor necrosis factor alpha. Nuclear Akt associates with p300 and phosphorylates its Ser-1834 both in vivo and in vitro. The phosphorylation induces recruitment of p300 to the ICAM-1 promoter, leading to the acetylation of histones in chromatin and association with the basal transcriptional machinery RNA polymerase II. These two events facilitate ICAM-1 gene expression and are abolished by the p300 S1834A mutant, inhibitors of PI3K/Akt, or small interfering RNA of Akt. Histone acetylation is attributed to the Akt-enhanced intrinsic histone acetyltransferase (HAT) activity of p300 and its association with another HAT, p/CAF. Our study provides a new insight into the molecular mechanism by which Akt promotes the transcriptional potential of p300.
MeSH term(s)	Acetyltransferases/metabolism ; Cell Line, Tumor ; Histone Acetyltransferases ; Histones/metabolism ; Humans ; Intercellular Adhesion Molecule-1/biosynthesis ; Intercellular Adhesion Molecule-1/genetics ; Nuclear Proteins/metabolism ; Nucleosomes/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Serine/metabolism ; Trans-Activators/metabolism ; Transcription, Genetic/physiology ; Tumor Necrosis Factor-alpha/metabolism ; U937 Cells
Chemical Substances	Histones ; Nuclear Proteins ; Nucleosomes ; Proto-Oncogene Proteins ; Trans-Activators ; Tumor Necrosis Factor-alpha ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Serine (452VLY9402) ; Acetyltransferases (EC 2.3.1.-) ; Histone Acetyltransferases (EC 2.3.1.48) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; AKT1 protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2005-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.25.15.6592-6602.2005
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