Nitroprusside stimulates mitochondrial aconitase gene expression through the cyclic adenosine 3?,5?-monosphosphate signal transduction pathway in human prostate carcinoma cells

The Prostate ◽  
2004 ◽  
Vol 61 (1) ◽  
pp. 92-102 ◽  
Author(s):  
Horng-Heng Juang
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Prostate Carcinoma ◽  
Signal Transduction Pathway ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Transduction Pathway ◽  
Mitochondrial Aconitase ◽  
Human Prostate Carcinoma

p53 downregulates the gene expression of mitochondrial aconitase in human prostate carcinoma cells

The Prostate ◽  
2010 ◽  
Vol 71 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Ke-Hung Tsui ◽  
Tsui-Hsia Feng ◽  
Yu-Fen Lin ◽  
Phei-Lang Chang ◽  
Horng-Heng Juang
Keyword(s):  
Gene Expression ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Mitochondrial Aconitase ◽  
Human Prostate Carcinoma

Gene expression changes in human prostate carcinoma cells exposed to genotoxic and nongenotoxic aryl hydrocarbon receptor ligands

2011 ◽  
Vol 206 (2) ◽  
pp. 178-188 ◽  
Author(s):  
Eva Hrubá ◽  
Jan Vondráček ◽  
Helena Líbalová ◽  
Jan Topinka ◽  
Vítězslav Bryja ◽  
...  
Keyword(s):  
Gene Expression ◽  
Aryl Hydrocarbon Receptor ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Receptor Ligands ◽  
Aryl Hydrocarbon ◽  
Human Prostate Carcinoma

scholarly journals Alterations in the focal adhesion kinase/Src signal transduction pathway correlate with increased migratory capacity of prostate carcinoma cells

Oncogene ◽  
2001 ◽  
Vol 20 (10) ◽  
pp. 1152-1163 ◽  
Author(s):  
Jill K Slack ◽  
Reid B Adams ◽  
Joshua D Rovin ◽  
Eric A Bissonette ◽  
Catherine E Stoker ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Prostate Carcinoma ◽  
Signal Transduction Pathway ◽  
Carcinoma Cells ◽  
Transduction Pathway ◽  
Migratory Capacity

scholarly journals Hypoxia upregulates the gene expression of mitochondrial aconitase in prostate carcinoma cells

2013 ◽  
Vol 51 (1) ◽  
pp. 131-141 ◽  
Author(s):  
Ke-Hung Tsui ◽  
Li-Chuan Chung ◽  
Shyi-Wu Wang ◽  
Tsui-Hsia Feng ◽  
Phei-Lang Chang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Carcinoma ◽  
Fatty Acid Synthase ◽  
Molecular Mechanisms ◽  
Transient Gene Expression ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Translation Initiation Site ◽  
Transcriptional Level ◽  
Mitochondrial Aconitase

Hypoxia induces metabolic alteration in cancer cells by stabilizing hypoxia-inducible factor 1α (HIF-1α (HIF1A)), which regulates the bioenergetic genes of glycolysis and lipid metabolic pathways. However, the target genes of hypoxia-induced metabolic alterations in the prostate remain uncertain. Mitochondrial aconitase (mACON) (ACONM) is an enzyme that is central to carbohydrate and energy metabolism and is responsible for the interconversion of citrate to isocitrate as part of the citric acid cycle in the human prostate. We evaluated the effects of the molecular mechanisms of hypoxia on mACON gene expression in PC-3 and LNCaP human prostate carcinoma cells. Immunoblotting assays revealed that hypoxia modulated mACON and lactate dehydrogenase A (LDHA) protein expression, while these effects were attenuated when HIF-1α was knocked down. Hypoxia induced fatty acid synthase (FASN) in PC-3 cells while hypoxia blocked FASN gene expression in LNCaP cells after 24-h incubation. Results of real-time RT-qPCR, immunoblotting, and transient gene expression assays revealed that hypoxia treatment or co-transfection with HIF-1α expression vector enhanced gene expression of mACON, implying that hypoxia modulated mACON at the transcriptional level. Hypoxia-induced mACON promoter activity is dependent on the DNA fragment located at −1013 to −842 upstream of the translation initiation site. l-mimosine, an iron chelator, stabilized HIF-1α but downregulated mACON gene expression, suggesting that iron chelation blocked the hypoxia-induced mACON gene expression. These results suggest that hypoxia dysregulates the expressions of LDHA, FASN, and mACON genes, and the hypoxia-induced mACON gene expression is via the HIF-1α-dependent and iron-dependent pathways in prostate carcinoma cells.

scholarly journals Thioredoxin-interacting protein: an oxidative stress-related gene is upregulated by glucose in human prostate carcinoma cells

2008 ◽  
Vol 42 (3) ◽  
pp. 205-214 ◽  
Author(s):  
See-Tong Pang ◽  
Wen-Chi Hsieh ◽  
Cheng-Keng Chuang ◽  
Chun-Hsiang Chao ◽  
Wen-Hui Weng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glucose Metabolism ◽  
Prostate Carcinoma ◽  
Promoter Activity ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Response Element ◽  
Interacting Protein ◽  
Thioredoxin Interacting Protein ◽  
Human Prostate Carcinoma

Thioredoxin-interacting protein (TXNIP), also known as vitamin-D3 upregulated protein 1, interacts with reduced thioredoxin. This protein modulates the cellular redox state and plays a role in stress-induced cellular apoptosis. This study examined TXNIP gene expression in prostate cancer cells. In vitro studies by immunoblot assay have shown that elevated glucose levels (1–15 mM) upregulate TXNIP gene expression two- to fourfold in human prostate carcinoma cells (LNCaP) and hepatocellular carcinoma cells (HepG2). Transient gene expression assays reveal that the promoter activity of the TXNIP gene is upregulated by glucose, 3-O-methylglucose, and maltose, but not by mannitol. These results suggest that glucose and 3-O-methylglucose induce TXNIP expression through both glucose metabolism-dependent and -independent pathways. Cotransfection of a plasmid expression carbohydrate response element-binding protein (ChREBP) with a TXNIP reporter vector into LNCaP cells dramatically enhances reporter activity in a low glucose (1 mM) condition. The effects of glucose are apparently mediated in a region located −341 to −324 bp upstream of the translational starting point of the TXNIP gene as indicated by 5′-deletion and site-directed mutagenesis reporter assays. Mutation of the putative carbohydrate response element (ChoRE) from CACGAGGGCAGCACGAG to TTTGAGGGCAGCACGAG abolishes glucose upregulation of TXNIP promoter activity. The present study demonstrates that TXNIP is transcription induced in both LNCaP and HepG2 cells in an increased glucose metabolism-dependent or -independent response, and a putative glucose regulatory system including ChREBP and ChoRE is needed for glucose-induced TXNIP gene in human prostate carcinoma cells.

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