foxm1 inhibitor rcm 1 Search Results


94
MedChemExpress rcm 1
A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the <t>FOXM1</t> mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
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92
Bio-Techne corporation rcm 1
A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the <t>FOXM1</t> mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
Rcm 1, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Selleck Chemicals foxm1 inhibitor rcm
A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the <t>FOXM1</t> mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
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90
Tocris rcm1 inhibitors
A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the <t>FOXM1</t> mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
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Image Search Results


A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the FOXM1 mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Cell Death Discovery

Article Title: Down-regulated m6A reader FTO destabilizes PHF1 that triggers enhanced stemness capacity and tumor progression in lung adenocarcinoma

doi: 10.1038/s41420-022-01125-y

Figure Lengend Snippet: A Gene set enrichment analysis (GSEA) was conducted to compare the enriched pathways in PHF1-low and PHF1-high groups. B Tumorsphere images of LUAD CSCs in parental WT and PHF1-KO groups (Scale bar = 200 μm). Quantification was shown on the right. C In vitro limiting dilution analysis of the tumorsphere formations of LUAD CSCs (WT & KO#1). PHF1 deficiency enhanced the self-renewal capacity of LUAD CSCs. D The qPCR assay screening the representative stemness-associated signature in parental and PHF1-KO A549 cells. E The qPCR assay detecting the FOXM1 mRNA levels in LUAD cells (A549, H1299) transfected with vetctor and PHF1. F ChIP-qPCR assays were performed to detect the enrichment of PHF1 and corresponding H3K36me3 at the promoter loci of FOXM1. G Gene correlation analysis was conducted with Spearson statistics between PHF1 and FOXM1 based on the TCGA-LUAD cohort. H CCK-8 assay was conducted to detect the in vitro cell growth in PHF1-deficient cells infected with shCtrl or shFOXM1. I The qPCR assay was conducted to detect the relative FOXM1 mRNA levels in FTO-KD cells transfected with vector or PHF1. J CCK-8 assay was performed to detect the in vitro cell growth in FTO-KD cells infected with shCtrl or shFOXM1. K Representative images of mice with xenografts tumors derived from H1299 cells. L Quantification of tumor volumes at indicated timepoints in the above subcutaneous model. Bar = Mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The RCM-1 (FOXM1 inhibitor) was obtained from the MCE company.

Techniques: In Vitro, Transfection, CCK-8 Assay, Infection, Plasmid Preparation, Derivative Assay