The Experts below are selected from a list of 25281 Experts worldwide ranked by ideXlab platform
Ercan Kurar - One of the best experts on this subject based on the ideXlab platform.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.
Marie Mcdonald - One of the best experts on this subject based on the ideXlab platform.
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De Novo Pathogenic Variants in N-cadherin Cause a Syndromic Neurodevelopmental Disorder with Corpus Callosum, Axon, Cardiac, Ocular, and Genital Defects
American Journal of Human Genetics, 2019Co-Authors: Andrea Accogli, Sara Calabretta, Judith St-onge, Nassima Boudrahem-addour, Alexandre Dionne-laporte, Pascal Joset, Silvia Azzarello-burri, Anita Rauch, Juan Pallais, Marie McdonaldAbstract:Cadherins constitute a family of transmembrane proteins that mediate calcium-dependent cell-cell adhesion. The extracellular domain of cadherins consists of extracellular cadherin (EC) domains, separated by calcium binding sites. The EC interacts with other cadherin molecules in cis and in trans to mechanically hold apposing cell surfaces together. CDH2 encodes N-cadherin, whose essential roles in neural development include neuronal migration and axon pathfinding. However, CDH2 has not yet been linked to a Mendelian neurodevelopmental disorder. Here, we report de novo heterozygous pathogenic variants (seven missense, two frameshift) in CDH2 in nine individuals with a syndromic neurodevelopmental disorder characterized by global developmental delay and/or intellectual disability, variable axon pathfinding defects (corpus callosum agenesis or hypoplasia, mirror movements, Duane anomaly), and ocular, cardiac, and genital anomalies. All seven missense variants (c.1057G>A [p.Asp353Asn]; c.1789G>A [p.Asp597Asn]; c.1789G>T [p.Asp597Tyr]; c.1802A>C [p.Asn601Thr]; c.1839C>G [p.Cys613Trp]; c.1880A>G [p.Asp627Gly]; c.2027A>G [p.Tyr676Cys]) result in substitution of highly conserved residues, and six of seven cluster within EC domains 4 and 5. Four of the substitutions affect the calcium-binding site in the EC4-EC5 interdomain. We show that cells expressing these variants in the EC4-EC5 domains have a defect in cell-cell adhesion; this defect includes impaired binding in trans with N-cadherin-WT expressed on apposing cells. The two frameshift variants (c.2563_2564delCT [p.Leu855Valfs∗4]; c.2564_2567dupTGTT [p.Leu856Phefs∗5]) are predicted to lead to a truncated cytoplasmic domain. Our study demonstrates that de novo heterozygous variants in CDH2 impair the adhesive activity of N-cadherin, resulting in a multisystemic developmental disorder, that could be named ACOG syndrome (agenesis of corpus callosum, axon pathfinding, cardiac, ocular, and genital defects).
Canan Eroglu - One of the best experts on this subject based on the ideXlab platform.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.
Andrea Accogli - One of the best experts on this subject based on the ideXlab platform.
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De Novo Pathogenic Variants in N-cadherin Cause a Syndromic Neurodevelopmental Disorder with Corpus Callosum, Axon, Cardiac, Ocular, and Genital Defects
American Journal of Human Genetics, 2019Co-Authors: Andrea Accogli, Sara Calabretta, Judith St-onge, Nassima Boudrahem-addour, Alexandre Dionne-laporte, Pascal Joset, Silvia Azzarello-burri, Anita Rauch, Juan Pallais, Marie McdonaldAbstract:Cadherins constitute a family of transmembrane proteins that mediate calcium-dependent cell-cell adhesion. The extracellular domain of cadherins consists of extracellular cadherin (EC) domains, separated by calcium binding sites. The EC interacts with other cadherin molecules in cis and in trans to mechanically hold apposing cell surfaces together. CDH2 encodes N-cadherin, whose essential roles in neural development include neuronal migration and axon pathfinding. However, CDH2 has not yet been linked to a Mendelian neurodevelopmental disorder. Here, we report de novo heterozygous pathogenic variants (seven missense, two frameshift) in CDH2 in nine individuals with a syndromic neurodevelopmental disorder characterized by global developmental delay and/or intellectual disability, variable axon pathfinding defects (corpus callosum agenesis or hypoplasia, mirror movements, Duane anomaly), and ocular, cardiac, and genital anomalies. All seven missense variants (c.1057G>A [p.Asp353Asn]; c.1789G>A [p.Asp597Asn]; c.1789G>T [p.Asp597Tyr]; c.1802A>C [p.Asn601Thr]; c.1839C>G [p.Cys613Trp]; c.1880A>G [p.Asp627Gly]; c.2027A>G [p.Tyr676Cys]) result in substitution of highly conserved residues, and six of seven cluster within EC domains 4 and 5. Four of the substitutions affect the calcium-binding site in the EC4-EC5 interdomain. We show that cells expressing these variants in the EC4-EC5 domains have a defect in cell-cell adhesion; this defect includes impaired binding in trans with N-cadherin-WT expressed on apposing cells. The two frameshift variants (c.2563_2564delCT [p.Leu855Valfs∗4]; c.2564_2567dupTGTT [p.Leu856Phefs∗5]) are predicted to lead to a truncated cytoplasmic domain. Our study demonstrates that de novo heterozygous variants in CDH2 impair the adhesive activity of N-cadherin, resulting in a multisystemic developmental disorder, that could be named ACOG syndrome (agenesis of corpus callosum, axon pathfinding, cardiac, ocular, and genital defects).
Hasibe Vural - One of the best experts on this subject based on the ideXlab platform.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.
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anticancer mechanism of sinapic acid in pc 3 and lncap human prostate cancer cell lines
Gene, 2018Co-Authors: Canan Eroglu, Ebru Avci, Hasibe Vural, Ercan KurarAbstract:Abstract Sinapic acid (SA) is a derivative of hydroxycinnamic acid and found in various vegetables and fruit species. Aim was to evaluate the anticancer effects of SA in PC-3 and LNCaP human prostate cancer cells. The effect of SA on cell viability was determined using XTT assay. Expressions of 8 genes for apoptosis and 6 genes for metastasis were evaluated by qPCR. Caspase-3 activity was determined using caspase-3 colorimetric assay kit. Effect of SA on cell invasion was evaluated with cell invasion assay. The IC50 dose of SA in PC-3 and LNCaP cells was found to be 1000 μM for 72 h. SA treatment increased the expression of BAX, CASP3, CASP8, CYCS, FAS, TIMP-1 and CDH1 however significantly decreased the expression of MMP-9 in PC-3 cells. In LNCaP cells, the expressions of BAX, CASP3, CASP7 and CYCS were significantly elevated; however, a decrease was seen in the expressions of CDH2, MMP-2 and MMP-9 in the SA treatment. Moreover, SA significantly increased caspase-3 activity and suppressed the cell invasion. In conclusion, it is thought that SA has anticancer effect on prostate cancer cells. However, more detailed studies should be conduct to illuminate molecular mechanism of apoptotic and antimetastatic activity of SA.