Project description:FOXM1 plays a key role in M phase in normal cells and is overexpressed in human glioma. We found that FOXM1 deprivation could sensitize the glioma cells to TMZ chemotherapy. To find out the mechanistic regulation of FOXM1 in chemo-resistant genes, we used microarrays to select the potential genes regulated by FOXM1 which dominates in glioma chemo-resistance. U87 glioma cells were transiently transfected with none-target siRNA or FOXM1 siRNA. Total RNA were extracted after 48 hours and subjected to the microarray.
Project description:We performed microarray analysis in order to evaluate the effect of ONC201 and its derivatives (ONC206 and ONC212) on gene expression in U87 glioma cells.
Project description:We have employed whole RNA microarray expression profiling as a discovery platform to identify genes regulated by overexpression of miR-145 in U87 glioma cell. Lentivirus containing miR-145 coding sequence was infected to U87 cell to make U87 overexpressing miR-145. We did genome microarray between U87 and U87 overexpressing miR-145.
Project description:Microarray expression profiling of mRNAs using RNA extracted from miR-151a-overexpressing and miR-NC overexpressing U87 glioma cells.
Project description:An experimental lung metastasis assay was used to derive an invasive subline of U87 that is metastatic in mice. We used microarray analyses to find out over-represented gene ontologies that can explain the observed enhanced invasiveness of U87-2M1 cells. Early passage U87-2M1 cells and parental U87 glioma cells from ATCC were selected for RNA extraction and hybridization on microarray
Project description:Glioma is characterized by high migration and invasion, and the relative molecular mechanism is still poor. Accumulating studies demonstrated that ubiquitin specific protease 39 (USP39) played an oncogenic role in several cancers. Here, we investigate USP39 expression and function in human glioma. Oncomine database analysis revealed high USP39 expression in glioma and elevated USP39 expression correlated significantly with poor overall survival. Knockdown of USP39 significantly inhibited the migration and invasion of U251 and U87 cells. The gene expression profile was executed to screen the target molecules of USP39. The result showed that ADAM9, a molecule involved in migration and invasion of various human tumors, was significantly downregulated in the U251 and U87 cells with shRNA-mediated USP39 knockdown. Mechanistically, USP39 directly interacted with the ADAM9 mRNA and induced ADAM9 mRNA maturation, following the decreased expression of integrin β1. Besides, overexpressed ADAM9 rescued the inhibited migration and invasion of glioma cells causing by USP39 depletion. USP39 promoted invasion in vivo and reduced the overall survival of the mice. Collectively, USP39 may have oncogenic role that increase ADAM9 protein levels by inducing maturation of ADAM9 mRNA in glioma. USP39 could be considered a new potential therapeutic target for glioma.
Project description:FOXM1 plays a key role in M phase in normal cells and is overexpressed in human glioma. We found that FOXM1 deprivation could sensitize the glioma cells to TMZ chemotherapy. To find out the mechanistic regulation of FOXM1 in chemo-resistant genes, we used microarrays to select the potential genes regulated by FOXM1 which dominates in glioma chemo-resistance.
