mmp 7 Search Results


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R&D Systems elisa kit
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R&D Systems human total mmp 7
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R&D Systems anti human pe conjugated mmp 7
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Addgene inc expression plasmid pcdna3 gfp mmp 7
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Cell Signaling Technology Inc mmp7 3801s
Figure 3 FAM110B downregulated p-GSK-3β, active β-catenin, Cyclin B1, Cyclin D1, MMP2 and <t>MMP7.</t> Using indicated antibodies, Western blotting assay in A549 and H1299 cells after transfecting with FAM110B plasmid (A, B) and FAM110B siRNA (C, D). *P < 0.05, **P < 0.01 (Vec, Vector; 110B, FAM110B; si110B, siFAM110B).
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Cell Signaling Technology Inc mmp7
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
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Proteintech mmp 7
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
Mmp 7, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94
Santa Cruz Biotechnology anti mmp 7
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
Anti Mmp 7, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology mmp 7
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
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R&D Systems monoclonal antibody against human pro matrilysin
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
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R&D Systems metalloproteinase 7
Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; <t>MMP7,</t> matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.
Metalloproteinase 7, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Figure 3 FAM110B downregulated p-GSK-3β, active β-catenin, Cyclin B1, Cyclin D1, MMP2 and MMP7. Using indicated antibodies, Western blotting assay in A549 and H1299 cells after transfecting with FAM110B plasmid (A, B) and FAM110B siRNA (C, D). *P < 0.05, **P < 0.01 (Vec, Vector; 110B, FAM110B; si110B, siFAM110B).

Journal: OncoTargets and Therapy

Article Title:

FAM110B Inhibits Non-Small Cell Lung Cancer Cell Proliferation and Invasion Through Inactivating Wnt/β-Catenin Signaling

doi: 10.2147/ott.s247491

Figure Lengend Snippet: Figure 3 FAM110B downregulated p-GSK-3β, active β-catenin, Cyclin B1, Cyclin D1, MMP2 and MMP7. Using indicated antibodies, Western blotting assay in A549 and H1299 cells after transfecting with FAM110B plasmid (A, B) and FAM110B siRNA (C, D). *P < 0.05, **P < 0.01 (Vec, Vector; 110B, FAM110B; si110B, siFAM110B).

Article Snippet: The following primary Variables Number of Patients (%) Number 183 Age (years) <60 72(39.34) ≥60 111(60.66) Gender Male 112(61.20) Female 71(38.80) Histological type Squamous cell carcinoma 66(36.07) Adenocarcinoma 115(62.84) Large cell carcinoma 2(1.09) Differentiation Well 75(40.98) Moderate & poor 108(59.02) TNM classification I 67(36.61) II 71(38.80) III 45(24.59) Lymph node metastasis Positive 85(46.45) Negative 98(53.55) Smoking history Never 97(53.01) Ever 86(46.99) EGFR mutation Negative 110(60.11) Positive 73(39.89) OncoTargets and Therapy 2020:13 submit your manuscript | www.dovepress.com DovePress 4375 O nc oT ar ge ts a nd T he ra py d ow nl oa de d fr om h ttp s: //w w w .d ov ep re ss .c om / b y 93 .1 77 .1 19 .1 50 o n 20 -J un -2 02 0 F or p er so na l u se o nl y. Powered by TCPDF (www.tcpdf.org) 1 / 1 antibodies were used to incubate membranes at 4°C overnight: MYC-tag (2276S), β-catenin (S33/S37/ Thr41; 8814S), p-β-catenin (S33/S37/ST41; 9561S), GSK-3β (12456S), p-GSK-3β (S9; 5558S), Cyclin B1 (4135S), Cyclin D1 (2978S), MMP2 (40994S), MMP7 (3801S) (1:1000; Cell Signaling Technology Danvers, MA, USA); FAM110B (1:1000, Sigma); GAPDH (1:1000, Sigma, St.Louis, MO; USA).

Techniques: Western Blot, Plasmid Preparation

Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; MMP7, matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.

Journal: Biochimica et biophysica acta

Article Title: Cyclopeptide RA-V inhibits cell adhesion and invasion in both estrogen receptor positive and negative breast cancer cells via PI3K/AKT and NF-κB signaling pathways.

doi: 10.1016/j.bbamcr.2015.04.020

Figure Lengend Snippet: Fig. 1. (A) Chemical structure of cyclopeptide RA-V. (B–E) Data of microarray analysis. (B) The heatmap of differential expressed genes in RA-V treated and untreated control samples (n = 3). Hierarchical cluster analysis was carried out for all differential expressed genes (fold change ≥2 or ≤0.5; p value b 0.05) in RA-V-treated Hela cells, compared with the untreated control. Each column represented one sample. Red colored columns indicated up-regulated genes while green colored columns indicated down-regulated genes. (C) Hierarchical cluster analysis showed the differential expressions of tumor metastasis-related genes induced by RA-V. Each column represented one sample and each row represented one gene. The scale of color intensity was positively correlated to the fold change. (IGFBP6, insulin-like growth factor binding protein 6; ECM2, extracellular matrix protein 2; ICAM4, intercellular adhesion mol- ecule 4; TIMP4, tissue inhibitor of metalloproteinase 4; ICAM3, intercellular adhesion molecule 3; ICAM5, intercellular adhesion molecule 5; PLAU, urokinase-plasminogen activator; ITGA2B, integrin, alpha 2b; LAMA3, laminin, alpha 3; ALDH3A2, aldehyde dehydrogenase 3 family, member A2; TP53, tumor protein p53; LAMB3, laminin, beta 3; ALDH5A1, aldehyde dehydrogenase 5 family, member A1; ALDH3B1, aldehyde dehydrogenase 3 family, member B1; IGFLR1, IGF-like family receptor 1; COL1A1, collagen, type I, alpha 1; CFL2, cofilin 2; MMP15, matrix metallopeptidase 15; ID1, inhibitor of DNA binding 1; IGSF8, immunoglobulin superfamily, member 8; ID3, inhibitor of DNA binding 3; TIMP3, tissue inhibitor of metal- loproteinase 3; ALDH16A1, aldehyde dehydrogenase 16 family, member A1; MMP28, matrix metallopeptidase 28; IGSF3, immunoglobulin superfamily, member 3; LAMB2, laminin, beta 2; COL4A5, collagen, type IV, alpha 5; COL4A4, collagen, type IV, alpha 4; IGFL2, IGF-like family member 2; TNC, tenascin C; IGF2BP1, insulin-like growth factor 2 mRNA binding protein 1; LAMA2, laminin, alpha 2; MMP7, matrix metallopeptidase 7; MMP19, matrix metallopeptidase 19; ITGB8, integrin, beta 8; ITGAM, integrin, alpha M; LAMB1, laminin, beta 1; r, laminin, gamma 2). (D) RA-V induced cancer invasion and metastasis-associated GO categories. GO categories cover 3 domains, cellular component, molecular function and biological process. Genes with differential expressions were analyzed and subjected to GO analysis in accordance with the SBC Analysis System. GO categories (p value b 0.05; Hit ≥5) were considered to be significant. ‘Hits’ was considered as the number of the differential expressed genes according to each GO category. (E) Table showed the top 5 signaling pathways involved in Hela cells in response to RA-V. aThe number of the differential expressed genes in a pathway according to Biocarta and Kegg databases. bThe enrichment p value of the pathway as de- termined by R-package Fisher's Exact Test.

Article Snippet: The blots were incubated with primary antibodies, betaactin (Sigma, USA), MMP1, MMP2, MMP7, MMP9, uPA, TIMP-1, ER, ROCK1, pEGFR, EGFR (Abcam, USA), cofilin, p-cofilin, Cdc42, RhoA, TIMP-2, PI3K, pPI3K, AKT, pAKT, FAK, NF-κB, pNF-κB, IκB and pIκB (Cell Signalling, USA) overnight.

Techniques: Microarray, Control, Binding Assay, Protein-Protein interactions