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| 1 | Pea3 expression promotes the invasive and metastatic potential of colorectal carcinoma显示文摘AIM:To investigate the function of Pea3 in colorectal carcinoma(CRC)invasion and metastatic potential.METHODS:The expression of Pea3 during clinical progression of human CRC was investigated using Oncomine Research Edition.To assay Pea3 expression in established CRC cell lines,we performed western blotting of cell lysates.We employed sh RNA-mediated knockdown of Pea3 in HCT116(HCT)and LS174T CRC cells which was confirmed by real-time quantitative PCR(q PCR)and western blotting.Transwell invasion assays,MTS proliferation assays,anoikis assays,and fluorometric matrix metalloprotease(MMP)assays wereperformed to determine the effects of Pea3 knockdown on invasion,proliferation,anoikis and MMP activity in CRC cells in vitro.Alterations in epithelial-mesenchymal transition(EMT)and matrix metalloprotease(MMP)m RNA levels were determined by q PCR.CRC cells were injected into the flanks of nude mice to generate xenografts and tumor growth monitored with serial calliper measurements.To assay metastatic potential,CRC cells were injected into the spleen of nude mice,and histological analysis performed on the livers 21 d later.RESULTS:We demonstrated that reduction of Pea3expression in CRC cells significantly impaired their invasive capacity(HCT.sh Pea3,0.28±0.04 fold,P<0.01;LS.sh Pea3,0.15±0.04 fold;SW.sh Pea3,0.23±0.03,P<0.01),reduced anoikis resistance(HCT.sh Pea3 75.4%±1.9%viable cells vs HCT.sh Ctrl 88.6%±0.6%viable cells,P<0.01;LS.sh Pea3 71.7%±0.5%viable cells vs LS.Ctrl 89.6%±0.3%viable cells,P<0.005,but had no effect on proliferation(HCT.sh Ctrl AUC 5098±123 vs HCT.sh Pea3 5689±151,P<0.05;LS.sh Ctrl AUC 5600±324.1 vs LS.sh Pea3 6423±400,P<0.05).In vivo,HCT.sh Pea3 and HCT.sh Ctrl tumour xenografts grew at a similar rate(HCT.sh Pea3 2.64±0.82 fold vs HCT.sh Ctrl 2.88±0.80 fold,P>0.05).In keeping with a pro-metastatic function for Pea3 in CRC,several EMT markers and MMPs were downregulated in sh Pea3-expressing cells,suggesting that Pea3 may exert its effects through these processes.A reduction in overall MMP activity was observed in HCT.sh Pea3 cells compared to their control counterparts(HCT.sh Pea30.61±0.04 fold,P<0.005).This translated in vivo to the complete absence of metastases in the livers of mice that were grafted with CRC cells lacking Pea3.Conversely,CRC cells expressing Pea3 formed liver metastases in all mice.CONCLUSION:Our study implicates Pea3 as a mediator of metastases,and provides a biological rationale for the adverse prognosis associated with elevated Pea3 expression in human CRC. | Aruz Mesci Samira Taeb Xiaoyong Huang Rishi Jairath Darshan Sivaloganathan Stanley K Liu | 2014 | World Journal of Gastroenterology2014，20，46： | 7 |
| 2 | Resveratrol and fenofibrate ameliorate fructose-induced nonalcoholic steatohepatitis by modulation of genes expression显示文摘AIM: To evaluate the effect of resveratrol, alone and in combination with fenofibrate, on fructose-induced metabolic genes abnormalities in rats. METHODS: Giving a fructose-enriched diet(FED) to rats for 12 wk was used as a model for inducing hepatic dyslipidemia and insulin resistance. Adult male albino rats(150-200 g) were divided into a control group and a FED group which was subdivided into 4 groups, a control FED, fenofibrate(FENO)(100 mg/kg), resveratrol(RES)(70 mg/kg) and combined treatment( FENO + RES)( half the doses). A l l treatments were given orally from the 9th week till the end of experimental period. Body weight, oral glucose tolerance test(OGTT), liver index, glucose, insulin, insulin resistance(HOMA), serum and liver triglycerides(TGs), oxidative stress(liver MDA, GSH and SOD),serum AST, ALT, AST/ALT ratio and tumor necrosis factor-α(TNF-α) were measured. Additionally, hepatic gene expression of suppressor of cytokine signaling-3(SOCS-3), sterol regulatory element binding protein-1c(SREBP-1c), fatty acid synthase(FAS), malonyl Co A decarboxylase(MCD), transforming growth factor-β1(TGF-β1) and adipose tissue genes expression of leptin and adiponectin were investigated. Liver sections were taken for histopathological examination and steatosis area were determined.RESULTS: Rats fed FED showed damaged liver, impairment of glucose tolerance, insulin resistance, ox ida t ive s t re s s a nd dy s l ipide m ia. As fo r ge ne expression, there was a change in favor of dyslipidemia and nonalcoholic steatohepatitis(NASH) development. All treatment regimens showed some benefit in reversing the described deviations. Fructose caused deterioration in hepatic gene expression of SOCS-3, SREBP-1c, FAS, MDA and TGF-β1 and in adipose tissue gene expression of leptin and adiponectin. Fructose showed also an increase in body weight, insulin resistance(OGTT, HOMA), serum and liver TGs, hepatic MDA, serum AST, AST/ALT ratio and TNF-α compared to control. All treatments improved SOCS-3, FAS, MCD, TGF-β1 and leptin genes expression while only RES and FENO + RES groups showed an improvement in SREBP-1c expression. Adiponectin gene expression was improved only by RES. A decrease in body weight, HOMA, liver TGs, AST/ALT ratio and TNF-α were observed in all treatment groups. Liver index was increased in FENO and FENO + RES groups. Serum TGs was improved only by FENO treatment. Liver MDA was improved by RES and FENO + RES treatments. FENO + RES group showed an increase in liver GSH content.CONCLUSION: When resveratrol was given with half the dose of fenofibrate it improved NASH-related fructose-induced disturbances in gene expression similar to a full dose of fenofibrate. | Enas A Abd El-Haleim Ashraf K Bahgat Samira Saleh | 2016 | World Journal of Gastroenterology2016，22，10： | 5 |
| 3 | In vitro digestibility of bioactive peptides derived from bovine β- lactoglobulin 显示文摘 | Samira Rou k Sylvie F Gauthier Sylvie L Turgeon | 2006 | Int Dairy J2006，16，： | 1 |
| 4 | Emotional granularity and social functioning in individuals with schizophrenia:an experience sampling study 显示文摘 | David K Julia V Samira K | 2014 | J Psychiat Res2014，53，1： | 1 |
| 5 | Residential energy consumption patterns:the case of Lebanon显示文摘 | Ahrnad H Samira I K | 2005 | International Journal of Energy Research2005，29，8： | 1 |
| 6 | Residential energy consumption patterns:the case of Lebanon显示文摘 | Ahmad H Samira I K | 2005 | International Journal of Energy Research2005，29，8： | 1 |
| 7 | Germination responses of Cymbopogon schoenanthus to salinity显示文摘 | Ayda K Mohamed N Samira S | 2011 | Acta Physiologiae Plan- tarum2011，33，： | 1 |
| 8 | Antibiotic resistance in Gram-negative bacteria isolated from fanned catWsh 显示文摘 | SAMIRA S HOANG N K LE THANH H J L | 2007 | Food Control2007，18，： | 1 |
| 9 | Conditioning DRASTIC model to simulate nilrate pollution case study: Hamadan - Bahar Plain 显示文摘 | Samira A Sayed F M Jahangir A K | 2011 | Environment Earth Science2011，63，6： | 1 |
| 10 | Application of SWAT model to investigate nitrate leaching in Hamadan-Bahar Watershed, Iran显示文摘 | A Samira A K Jahangir S F Mousavi | 2010 | Agriculture Ecosystems and Environment2010，139，4： | 1 |
| 11 | Long-Term Shedding of Infectious Epstein-Barr Virus after Infectious Mononucleosis显示文摘 | Samira F K Patrice M Jean-Paul B | 2006 | Journal of Infectious Diseases2006，191，6： | 1 |
| 12 | Applica- tion of SWAT Model to Investigate Nitrate Leaching in Hamadan-Bahar Watershed, Iran 显示文摘 | Samira A Jahangir A K Mousavi S F | 2010 | Agriculture Ecosystems& Environment2010，139，4： | 1 |
| 13 | Ion release fromexperimental Au-Pt-based metal-ceramic alloys显示文摘 | Johnson A Shiraishib T Samira K | 2010 | DentMater2010，26，7： | 1 |
| 14 | High-temperature refining of metallurgical-grade silicon:A review显示文摘 | MURRAY D J LEILI T K MARK L SAMIRA S MANSOOR B | 2012 | JOM2012，64，8： | 1 |
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