the_cancer_genome_atlas_glioblastoma_multiforme

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the_cancer_genome_atlas_glioblastoma_multiforme [2021/05/17 10:36]
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the_cancer_genome_atlas_glioblastoma_multiforme [2021/05/17 10:38] (current)
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-[[Gene expression analysis]] was performed in GBM tumor samples and normal controls from the hospital, [[The Cancer Genome Atlas Glioblastoma Multiforme]] ([[TCGA-GBM]]) cohort, and the [[Gene Expression Omnibus]] (GEO) database (GSE7696). [[Cell proliferation]], [[apoptosis]], Matrigel Transwell, colony formation, and cell cycle assays were performed in T98 G and U251 cells in vitro. An orthotopic U251 xenograft murine model was employed to test the effects of RP3-439F8.1 knockdown in vivo.+[[Gene expression analysis]] was performed in GBM tumor samples and normal controls from [[Kunming]], [[The Cancer Genome Atlas Glioblastoma Multiforme]] ([[TCGA-GBM]]) cohort, and the [[Gene Expression Omnibus]] (GEO) database (GSE7696). [[Cell proliferation]], [[apoptosis]], Matrigel Transwell, colony formation, and cell cycle assays were performed in T98 G and U251 cells in vitro. An orthotopic U251 xenograft murine model was employed to test the effects of RP3-439F8.1 knockdown in vivo.
  
 [[NR5A2]] was upregulated in the three independent GBM tumor cohorts. [[In vitro]], NR5A2 overexpression enhanced GBM cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating β-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice. Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. These findings were clinically validated by a positive correlation between RP3-439F8.1 and NR5A2 and a negative correlation between RP3-439F8.1 and miR-139-5p in GBM tumors. [[NR5A2]] was upregulated in the three independent GBM tumor cohorts. [[In vitro]], NR5A2 overexpression enhanced GBM cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating β-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice. Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. These findings were clinically validated by a positive correlation between RP3-439F8.1 and NR5A2 and a negative correlation between RP3-439F8.1 and miR-139-5p in GBM tumors.
  • the_cancer_genome_atlas_glioblastoma_multiforme.txt
  • Last modified: 2021/05/17 10:38
  • by administrador