Project description:We observed that high extracellular formate concentrations promote the in vitro invasiveness of glioblastoma (GBM) cells. To identify mechanistically, how formates promotes invasion we chose an unbiased approach of RNAseq.
Project description:To identify the biological pathways regulated by PARP3, RNAseq of the WT and PARP3-/- LN229 human glioblastoma cells were performed. Samples were collected from subconfluent cells for total RNA isolation and RNA sequencing
Project description:Purpose: Characterization of transcriptomic alterations upon HPS90 inhibition in human LN229 and T98G glioblastoma cells in vitro. Methods: LN229 and T98G glioblastoma cells were treated with 10 nM of the HSP90 inhibitor NW457 or the vehicle control for 24 h, and total RNA was subjected to 3' RNA sequencing. Results: Distinct transcriptomic alterations were observed, dominated by a transcriptional upregulation of the heat shock response. Conclusion: HSP90 inhibition resulted in distinct transcriptomic alterations and a clear upregulation of the heat shock response.
Project description:We report the application of unit of bortezomib and panobinostat on LN229 cell , and further explored the mechanism of drugs on GBM cells.
Project description:To systematically identify the function of S6K1 and S6K2 in glioblastoma cells, LN229 cells were stably transduced with Cas9, control non-targeting sgRNA (sgNT), or sgRNAs targeting S6K1 or S6K2. The cells were then transiently transfected with non-targeting siRNAs (siNT), or siRNA pools targeting S6K1 or S6K2. RNA sequencing was performed to compare cellular responses to inactivation of single or combination S6 kinases.
Project description:Glutamine is an important nutriment for cancer cell growth that provides biological sources for nucleic acid and fatty acid synthesis, but the role of glutaminolysis in signal transduction and glioblastoma (GBM) progression remains little known. Here, we investigated whether GDH1, a key glutamate dehydrogenase, affects the expression levels of signal transduction factors by mRNA expression profiling of wild-type and GDH1 knockdown cells of the glioblastoma cell line LN229 cells
Project description:Arsenic trioxide (ATO) treatment leads to activation of mRNA translation through the MAPK-interacting kinase (MNK) signaling pathway. Polysomal fractionation and microarray analysis allows for identification of transcripts undergoing active translation. We identified the genes differentially enriched in untreated and ATO treated fractions. In this dataset, we include expression data in untreated and ATO treated LN229 cells using either the total or polysomal RNA.
Project description:Glioblastoma multiforme is the most common and aggressive form of brain cancer. The use of oncolytic HSV-1 (oHSV) to selectively target brain cancer cells leading to their lytic destruction has shown to be very promising in a preclinical setting, but is lacking efficacy in clinical trials. Cyr61, a secreted extracellular matrix protein which functions to promote angiogenesis, migration, proliferation and tumorigenesis, was found to be upregulated rapidly following oHSV infection. Here we show, using microarray analysis, that Cyr61 expression leads to the induction of several genes with type 1 interferon function. We show that Cyr61 mediated type 1 IFN induction is through its interaction with integrin alpha6beta1 on the cell surface and results in oHSV inhibition, reducing the efficacy of this therapy. We used microarray to detail the global program of gene expression underlying Cyr61 mediated oncolytic HSV-1 inhibition and identified distinct classes of up-regulated genes during this process. Tetracycline-Inducible glioma cells expressing Cyr61 protein in the presence of doxycycline were treated with or without doxycycline for 24 hours. RNA was extracted and hybridized on Affymetrix microarray. Two groups: ± dox to induce cyr61, performed in triplicate.
