The Experts below are selected from a list of 1914 Experts worldwide ranked by ideXlab platform
Mengxiang Yang - One of the best experts on this subject based on the ideXlab platform.
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circular rna circ ACACA regulates proliferation migration and glycolysis in non small cell lung carcinoma via mir 1183 and pi3k pkb pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
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Circular RNA circ‑ACACA regulates proliferation, migration and glycolysis in non‑small‑cell lung carcinoma via miR‑1183 and PI3K/PKB pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
Wenwen Wu - One of the best experts on this subject based on the ideXlab platform.
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circular rna circ ACACA regulates proliferation migration and glycolysis in non small cell lung carcinoma via mir 1183 and pi3k pkb pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
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Circular RNA circ‑ACACA regulates proliferation, migration and glycolysis in non‑small‑cell lung carcinoma via miR‑1183 and PI3K/PKB pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
Wei Xi - One of the best experts on this subject based on the ideXlab platform.
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circular rna circ ACACA regulates proliferation migration and glycolysis in non small cell lung carcinoma via mir 1183 and pi3k pkb pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
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Circular RNA circ‑ACACA regulates proliferation, migration and glycolysis in non‑small‑cell lung carcinoma via miR‑1183 and PI3K/PKB pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
Huimin Li - One of the best experts on this subject based on the ideXlab platform.
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circular rna circ ACACA regulates proliferation migration and glycolysis in non small cell lung carcinoma via mir 1183 and pi3k pkb pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
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Circular RNA circ‑ACACA regulates proliferation, migration and glycolysis in non‑small‑cell lung carcinoma via miR‑1183 and PI3K/PKB pathway
International Journal of Molecular Medicine, 2020Co-Authors: Wenwen Wu, Wei Xi, Huimin Li, Mengxiang YangAbstract:: Non‑small cell lung carcinoma (NSCLC) accounts for 85% of all lung cancers and the five‑year survival rate is ~1% in the late stage. Circular RNAs (circRNAs) were reported to be involved in the progression of diverse human cancers. However, the role of circ‑ACACA in NSCLC progression remains elusive. Quantitative polymerase chain reaction was conducted to detect the expression levels of circ‑ACACA and microRNA (miR)‑1183 in NSCLC tissues and cells. A Cell Counting Kit‑8 assay and transwell assay were employed to check proliferation and migration, respectively. Metabolic alternations in NSCLC cells were monitored by the Seahorse XFe96 analyzer. The protein levels of cellular myelocytomatosis, matrix metallopeptidase 9, glucose transporter 1, phosphatase and tensin homolog, phosphoinositide 3‑kinases (PI3K), phosphorylated PI3K (p‑PI3K), protein kinase B (PKB) and p‑PKB in samples were measured by western blotting. The interaction between circ‑ACACA and miR‑1183 was predicted by circular RNA Interactome, which was verified by dual‑luciferase reporter assay, RNA immunoprecipitation assay and RNA pull‑down assay. Xenograft tumor model was established to investigate the biological roles of circ‑ACACA in vivo. The level of circ‑ACACA was markedly upregulated in NSCLC tissues and cells, which was contrary to the expression of miR‑1183. Knockdown of circ‑ACACA inhibited proliferation and migration of NSCLC cells and also reduced the glycolysis rate. In addition, miR‑1183 was a target of circ‑ACACA and its downregulation reversed circ‑ACACA silencing‑mediated inhibitory impact on NSCLC progression. Further studies indicated that circ‑ACACA regulated the PI3K/PKB pathway through interacting with miR‑1183 and downregulation of circ‑ACACA suppressed tumor growth. Knockdown of circ‑ACACA impeded NSCLC progression by sponging miR‑1183 and inactivating the PI3K/PKB signaling pathway.
F Napolitano - One of the best experts on this subject based on the ideXlab platform.
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the ACACA gene is a potential candidate gene for fat content in sheep milk
Animal Genetics, 2013Co-Authors: Bianca Moioli, Maria Carmela Scata, G De Matteis, G Annicchiarico, G Catillo, F NapolitanoAbstract:Summary No major gene has yet been reported in sheep that explains the variation of milk fat content. The coding region of the acetyl-CoA carboxylase alpha (ACACA) gene, which plays an important role in de novo fatty acid synthesis, had been investigated, but no non-synonymous mutations have been reported. In this study, the genomic regions encoding the three promoters of the ACACA gene were directly sequenced in 264 sheep of three different breeds, and 10 SNPs were identified. Allele frequencies of most SNPs significantly differed (P = 0.05–0.0001) between breeds. The SNPs that potentially altered either gene regulatory elements or putative binding sites of transcription factors were made evident through in silico analysis. The association analysis with milk traits, performed for one SNP of PIII (GenBank AJ292286, g.1330G>T), showed a significant allelic substitution effect (+0.33%, P < 0.0001 and +0.35%, P < 0.01) in the Altamurana and Gentile breeds respectively. Because this SNP was located in the binding site of the paired box protein transcription factors, which was shown to function as an efficient promoter element, and because PIII transcripts are expressed in the mammary gland, the SNP in PIII of the ACACA gene might affect the variation of fat content in sheep milk.
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The ACACA gene is a potential candidate gene for fat content in sheep milk
Animal Genetics, 2013Co-Authors: Bianca Moioli, Maria Carmela Scata, G De Matteis, G Annicchiarico, G Catillo, F NapolitanoAbstract:Summary No major gene has yet been reported in sheep that explains the variation of milk fat content. The coding region of the acetyl-CoA carboxylase alpha (ACACA) gene, which plays an important role in de novo fatty acid synthesis, had been investigated, but no non-synonymous mutations have been reported. In this study, the genomic regions encoding the three promoters of the ACACA gene were directly sequenced in 264 sheep of three different breeds, and 10 SNPs were identified. Allele frequencies of most SNPs significantly differed (P = 0.05–0.0001) between breeds. The SNPs that potentially altered either gene regulatory elements or putative binding sites of transcription factors were made evident through in silico analysis. The association analysis with milk traits, performed for one SNP of PIII (GenBank AJ292286, g.1330G>T), showed a significant allelic substitution effect (+0.33%, P
