References (9)

Title : Areca nut-induced buccal mucosa fibroblast contraction and its signaling: a potential role in oral submucous fibrosis--a precancer condition - Chang_2013_Carcinogenesis_34_1096
Author(s) : Chang MC , Lin LD , Wu HL , Ho YS , Hsien HC , Wang TM , Jeng PY , Cheng RH , Hahn LJ , Jeng JH
Ref : Carcinogenesis , 34 :1096 , 2013
Abstract : Betel quid (BQ) chewing is an oral habit that increases the risk of oral cancer and oral submucous fibrosis (OSF), a precancerous condition showing epithelial atrophy and tissue fibrosis. Persistent fibroblast contraction may induce the fibrotic contracture of tissue. In this study, we found that areca nut extract (ANE) (200-1200 microg/ml) stimulated buccal mucosa fibroblast (OMF)-populated collagen gel contraction. Arecoline but not arecaidine-two areca alkaloids, slightly induced the OMF contraction. Exogenous addition of carboxylesterase (2U/ml) prevented the arecoline- but not ANE-induced OMF contraction. OMF expressed inositol triphosphate (IP3) receptors. ANE-induced OMF (800 microg/ml) contraction was inhibited by U73122 [phospholipase C (PLC) inhibitor] and 2-aminoethoxydiphenyl borate (IP3 receptor antagonist), respectively. Ethylene glycol tetraacetic acid and verapamil, two calcium mobilization modulators, also suppressed the ANE-induced OMF contraction. ANE induced calcium/calmodulin kinase II and myosin light chain (MLC) phosphorylation in OMF. Moreover, W7 (a Ca(2+)/calmodulin inhibitor), HA1077 (Rho kinase inhibitor), ML-7 (MLC kinase inhibitor) and cytochalasin B (actin filament polymerization inhibitor) inhibited the ANE-induced OMF contraction. Although ANE elevated reactive oxygen species (ROS) level in OMF, catalase, superoxide dismutase and N-acetyl-l-cysteine showed no obvious effect on ANE-elicited OMF contraction. These results indicate that BQ chewing may affect the wound healing and fibrotic processes in OSF via inducing OMF contraction by ANE and areca alkaloids. AN components-induced OMF contraction was related to PLC/IP3/Ca(2+)/calmodulin and Rho signaling pathway as well as actin filament polymerization, but not solely due to ROS production.
ESTHER : Chang_2013_Carcinogenesis_34_1096
PubMedSearch : Chang_2013_Carcinogenesis_34_1096
PubMedID: 23349021

Title : Complete genome sequence of Mycobacterium fortuitum subsp. fortuitum type strain DSM46621 - Ho_2012_J.Bacteriol_194_6337
Author(s) : Ho YS , Adroub SA , Aleisa F , Mahmood H , Othoum G , Rashid F , Zaher M , Ali S , Bitter W , Pain A , Abdallah AM
Ref : Journal of Bacteriology , 194 :6337 , 2012
Abstract : Mycobacterium fortuitum is a member of the rapidly growing nontuberculous mycobacteria (NTM). It is ubiquitous in water and soil habitats, including hospital environments. M. fortuitum is increasingly recognized as an opportunistic nosocomial pathogen causing disseminated infection. Here we report the genome sequence of M. fortuitum subsp. fortuitum type strain DSM46621.
ESTHER : Ho_2012_J.Bacteriol_194_6337
PubMedSearch : Ho_2012_J.Bacteriol_194_6337
PubMedID: 23105073
Gene_locus related to this paper: mycfo-k0uty1 , mycfo-k0ui29 , mycfo-k0usf4 , mycfo-k0uze5 , mycfo-k0v239 , mycfo-k0uvp7 , mycfo-k0unt7 , mycfo-k0vpb8 , mycfo-k0vcg0

Title : Complete genome sequence of Mycobacterium vaccae type strain ATCC 25954 - Ho_2012_J.Bacteriol_194_6339
Author(s) : Ho YS , Adroub SA , Abadi M , Al Alwan B , Alkhateeb R , Gao G , Ragab A , Ali S , van Soolingen D , Bitter W , Pain A , Abdallah AM
Ref : Journal of Bacteriology , 194 :6339 , 2012
Abstract : Mycobacterium vaccae is a rapidly growing, nontuberculous Mycobacterium species that is generally not considered a human pathogen and is of major pharmaceutical interest as an immunotherapeutic agent. We report here the annotated genome sequence of the M. vaccae type strain, ATCC 25954.
ESTHER : Ho_2012_J.Bacteriol_194_6339
PubMedSearch : Ho_2012_J.Bacteriol_194_6339
PubMedID: 23105074
Gene_locus related to this paper: mycva-k0upd3 , mycva-k0uc60 , mycva-k0uqa3 , mycva-k0uvn5 , mycva-k0uyk5 , mycva-k0vby5 , mycva-k0vig8 , mycva-k0uz23 , mycva-k0v9r0 , mycva-k0uhx8

Title : Tea polyphenol (-)-epigallocatechin-3-gallate inhibits nicotine- and estrogen-induced alpha9-nicotinic acetylcholine receptor upregulation in human breast cancer cells - Tu_2011_Mol.Nutr.Food.Res_55_455
Author(s) : Tu SH , Ku CY , Ho CT , Chen CS , Huang CS , Lee CH , Chen LC , Pan MH , Chang HW , Chang CH , Chang YJ , Wei PL , Wu CH , Ho YS
Ref : Mol Nutr Food Res , 55 :455 , 2011
Abstract : SCOPE: The aim of this research was to explore whether the tea-polyphenol (-)-epigallocatechin-3-gallate (EGCG) could be used as a potential agent for blocking smoking (nicotine, Nic)- or hormone (estradiol, E2)-induced breast cancer cell proliferation through inhibition of a common signaling pathway. METHODS AND
RESULTS: To explore whether Nic (>0.1 muM, 24 h) and E2 (>1 nM, 24 h) significantly increased alpha9-nicotinic acetylcholine (alpha9-nicotinic acetylcholine receptor (nAChR)) mRNA and protein expression levels, real-time PCR and immunoblotting analysis experiments were performed in human breast cancer (MCF-7) cells. Luciferase promoter activity experiment was performed to test the alpha9-nAChR promoter activity affected by Nic, E2 or EGCG. The results indicate that treatment with EGCG (1 muM) profoundly decreases Nic- and E2-induced MCF-7 proliferation by down regulating alpha9-nAChR expression. The alpha9-nAChR promoter activity is significantly induced by 24-h treatment with Nic (10 muM) or E2 (10 nM) (>1.8 and approximately 2.3-fold, respectively) in MCF-7 cells. Pretreatment with EGCG eliminated the Nic- and E2-induced alpha9-nAChR promoter-dependent luciferase activity. We further demonstrate that combined treatment with EGCG profoundly inhibits [3H]-Nic/ alpha9-nAChR binding activity in breast cancer cells.
CONCLUSIONS: We found that the EGCG could be used as an agent for blocking smoking (Nic)- or hormone (E2)-induced breast cancer cell proliferation by inhibiting of alpha9-nAChR signaling pathway. This study reveals the novel antitumor mechanisms of EGCG, and these results may have significant applications for chemopreventive purposes in human breast cancer.
ESTHER : Tu_2011_Mol.Nutr.Food.Res_55_455
PubMedSearch : Tu_2011_Mol.Nutr.Food.Res_55_455
PubMedID: 21370452

Title : Crosstalk between nicotine and estrogen-induced estrogen receptor activation induces alpha9-nicotinic acetylcholine receptor expression in human breast cancer cells - Lee_2011_Breast.Cancer.Res.Treat_129_331
Author(s) : Lee CH , Chang YC , Chen CS , Tu SH , Wang YJ , Chen LC , Chang YJ , Wei PL , Chang HW , Chang CH , Huang CS , Wu CH , Ho YS
Ref : Breast Cancer Research Treat , 129 :331 , 2011
Abstract : The primary aim of this study was to elucidate the role of the estrogen receptor (ER), a transcription factor involved in the nicotine- and 17beta-estradiol (E2)-mediated up-regulation of alpha9-nAChR gene expression. A real-time polymerase chain reaction (PCR) assay was used to quantify the alpha9-nAChR mRNA expression levels of surgically isolated (n=339) and laser-capture microdissected tissues (ER+ versus ER-, n= 6 per group). Chromatin immunoprecipitation (ChIP) and luciferase-promoter activity assays were used to investigate the ER-mediated transcriptional regulation of alpha9-nAChR gene expression. We observed that breast tumors with higher alpha9-nAChR mRNA expression levels (i.e., a mean fold ratio in the tumor/normal-paired samples of greater than tenfold) were associated with the lowest 5-year disease-specific survival rate (50%, dead/alive= 4/4, total = 8 patients, P= 0.006), in contrast to breast tumors with low levels (i.e., a mean fold ratio of less than onefold) of alpha9-nAChR expression (88%, dead/alive= 3/22, total= 25 patients). Furthermore, higher alpha9-nAChR mRNA expression levels were preferentially detected in ER+ tumor tissues in comparison to ER- tumor tissues (ER+ versus ER- patients: n=160 vs. 72; mean fold ratios of alpha9-nAChR expression = 11 +/- 3 vs. 6.7 +/- 2.3 fold, respectively). In vitro promoter-binding assays demonstrated that the ER is a major transcription factor that mediates nicotine- and E2-induced up-regulation of alpha9-nAChR gene expression in MCF-7 cells. In conclusion, our data indicate that the ER plays a central role in mediating alpha9-nAChR gene up-regulation in response to either nicotine or E2 stimulation.
ESTHER : Lee_2011_Breast.Cancer.Res.Treat_129_331
PubMedSearch : Lee_2011_Breast.Cancer.Res.Treat_129_331
PubMedID: 20953833

Title : Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors - Shih_2010_J.Agric.Food.Chem_58_235
Author(s) : Shih YL , Liu HC , Chen CS , Hsu CH , Pan MH , Chang HW , Chang CH , Chen FC , Ho CT , Yang YY , Ho YS
Ref : Journal of Agricultural and Food Chemistry , 58 :235 , 2010
Abstract : Large-scale epidemiological cohort studies performed in the United States indicate that breast cancer risk is associated with active and passive smoking. As of yet, however, there is no direct evidence of antitumor effects by agents that block the effect of tobacco compound nicotine (Nic) on relevant nicotinic receptors (nAChR) involved in breast tumorigenesis. In the present study, the expression profiles of different nAChR subunits in the human breast cancer cell line (MDA-MB-231) were characterized by RT-PCR. Nic (>0.1 microM, 6 h) significantly increased alpha9-nAChR mRNA and protein expression levels in human breast cancer cells (MDA-MB-231 cells). On the other hand, combined treatment with luteolin (Lut, 0.5 microM) and quercetin (Que, 0.5 microM) profoundly decreased MDA-MB-231 proliferation by down-regulating alpha9-nAChR expression. MDA-MB-231 cells were cultured in soft agar to evaluate anchorage-independent colony formation; combined treatment of Lut+Que inhibited Nic-induced MDA-MB-231 colony formation. Interestingly, the number of colonies formed was profoundly reduced in alpha9-nAChR knockdown (Si alpha9) cells in the combined (Lut+Que)-treated group as compared to the relevant control groups. Such results show that Lut- or Que-induced antitransforming activities were not limited to specific inhibition of the alpha9-nAChR receptor. Both alpha5- and alpha9-nAChR appear to be important molecular targets for Lut- and Que-induced antitumor effects in human breast cancer cells.
ESTHER : Shih_2010_J.Agric.Food.Chem_58_235
PubMedSearch : Shih_2010_J.Agric.Food.Chem_58_235
PubMedID: 19921817

Title : PAF-acetylhydrolases - Derewenda_1999_Biochim.Biophys.Acta_1441_229
Author(s) : Derewenda ZS , Ho YS
Ref : Biochimica & Biophysica Acta , 1441 :229 , 1999
Abstract : Platelet-activating factor acetylhydrolases (PAF-AHs, EC constitute a unique subfamily of phospholipases A(2), specific for short acyl chains in the sn-2 position of the phospholipid. Their primary substrate is the platelet-activating factor, PAF, from which they cleave an acetyl moiety with concomitant release of lysoPAF. However, some acetylhydrolase will also hydrolyze other polar phospholipids with up to 6-carbons long acyl chains in the sn-2 position. PAF-acetylhydrolases are diverse enzymes, and the well-characterized isoforms are serine-dependent hydrolases, which do not require Ca(2+) for activity. Given the existence of two pools of PAF, intra- and extracellular, the acetylhydrolases can be divided into two subclasses: those found in the cytosol and enzymes secreted to blood plasma or other body fluids. Recent crystallographic studies shed new light on the complex structure-function relationships in PAF-AHs.
ESTHER : Derewenda_1999_Biochim.Biophys.Acta_1441_229
PubMedSearch : Derewenda_1999_Biochim.Biophys.Acta_1441_229
PubMedID: 10570251

Title : Clinical evaluation of C7 spinal nerve transection: 21 patients with at least 2 years' follow-up - Chuang_1998_Br.J.Plast.Surg_51_285
Author(s) : Chuang DC , Cheng SL , Wei FC , Wu CL , Ho YS
Ref : Br J Plast Surg , 51 :285 , 1998
Abstract : We have performed C7 spinal nerve transfer to treat root injury of the brachial plexus since 1989. Out of a total of 43 patients, 21 have been followed up for at least 2 years. Evaluation of the effect of C7 transection included clinical examination, intraoperative C7 stimulation, LIDO Workset machine and electrophysiological studies to test C7 innervated muscles, and histochemical analysis of the anterior and posterior division of the upper trunk using acetylcholinesterase stain. Nearly half of the study group (48%) reported no significant sensory changes and most patients (81%) did not notice any weakness of the limb following C7 transection. Some patients did experience sensory and motor abnormalities which were most frequent during the first postoperative month, improved during the 2nd month and in most cases resolved in the 3rd postoperative month. The only longer persistent abnormality was the triceps reflex, which becomes weak or absent. We also found that intraoperative C7 stimulation was a useful predictor of possible post-transection morbidity. Subclinical deficits, detected by the LIDO workset machine and by electro-physiological studies, were quite common. Histochemical analysis revealed that the posterior division of C7 had more motor fibres than the anterior division.
ESTHER : Chuang_1998_Br.J.Plast.Surg_51_285
PubMedSearch : Chuang_1998_Br.J.Plast.Surg_51_285
PubMedID: 9771346

Title : Brain acetylhydrolase that inactivates platelet-activating factor is a G-protein-like trimer - Ho_1997_Nature_385_89
Author(s) : Ho YS , Swenson L , Derewenda U , Serre L , Wei Y , Dauter Z , Hattori M , Adachi T , Aoki J , Arai H , Inoue K , Derewenda ZS
Ref : Nature , 385 :89 , 1997
Abstract : The platelet-activating factor PAF (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a potent lipid first messenger active in general cell activation, fertilization, inflammatory and allergic reactions, asthma, HIV pathogenesis, carcinogenesis, and apoptosis. There is substantial evidence that PAF is involved in intracellular signalling, but the pathways are poorly understood. Inactivation of PAF is carried out by specific intra- and extracellular acetylhydrolases (PAF-AHs), a subfamily of phospholipases A2 that remove the sn-2 acetyl group. Mammalian brain contains at least three intracellular isoforms, of which PAF-AH(Ib) is the best characterized. This isoform contains a heterodimer of two homologous catalytic subunits alpha1 and alpha2, each of relative molecular mass 26K, and a non-catalytic 45K beta-subunit, a homologue of the beta-subunit of trimeric G proteins. We now report the crystal structure of the bovine alpha1 subunit of PAF-AH(Ib) at 1.7 A resolution in complex with a reaction product, acetate. The tertiary fold of this protein is closely reminiscent of that found in p21(ras) and other GTPases. The active site is made up of a trypsin-like triad of Ser 47, His 195 and Asp 192. Thus, the intact PAF-AH(Ib) molecule is an unusual G-protein-like (alpha1/alpha2)beta trimer.
ESTHER : Ho_1997_Nature_385_89
PubMedSearch : Ho_1997_Nature_385_89
PubMedID: 8985254