rp3-439f8.1

Differences

This shows you the differences between two versions of the page.

Link to this comparison view

Both sides previous revision Previous revision
rp3-439f8.1 [2021/05/17 10:49]
administrador
rp3-439f8.1 [2021/05/17 10:51] (current)
administrador
Line 5: Line 5:
 [[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 [[T98G]] 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 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 [[T98G]] 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 study supports a tumorigenic role for RP3-439F8.1 in GBM through the RP3-439F8.1/miR-139-5p/NR5A2 axis The study supports a tumorigenic role for RP3-439F8.1 in GBM through the RP3-439F8.1/miR-139-5p/NR5A2 axis
 ((Qi J, Pan L, Yu Z, Ni W. The [[lncRNA]] [[RP3-439F8.1]] promotes GBM [[cell proliferation]] and progression by sponging [[miR-139-5p]] to upregulate [[NR5A2]]. Pathol Res Pract. 2021 Jan 2;223:153319. doi: 10.1016/j.prp.2020.153319. Epub ahead of print. PMID: 33991848.)) ((Qi J, Pan L, Yu Z, Ni W. The [[lncRNA]] [[RP3-439F8.1]] promotes GBM [[cell proliferation]] and progression by sponging [[miR-139-5p]] to upregulate [[NR5A2]]. Pathol Res Pract. 2021 Jan 2;223:153319. doi: 10.1016/j.prp.2020.153319. Epub ahead of print. PMID: 33991848.))
  • rp3-439f8.1.txt
  • Last modified: 2021/05/17 10:51
  • by administrador