Project description:Here we performed a microarray experiment on samples of adherent cultures of Human Glioblastoma Cancer Stem Like Cells (NCH421K cell line) expressing a shRNA targeting the transcription factor ZEB1 (shZEB1) or a control shRNA targeting GFP 72 hours after lentiviral infection. This resulted in the generation of a genome-wide mRNA expression pattern and quantification for these cells in the two conditions.
Project description:Recent methylome studies have located N6-methyladenosine (m6A) RNA modification on thousands of mammalian transcripts. However, its functional mechanism remains unclear. In this study, we examined the role of m6A methylation in mouse embryonic stem cells. To gain an understanding of dynamic changes in cells depleted with (proposed) methyltranferases at molecular level, we examined the time-series gene expression pattern in mESC lines using microarray analysis. After 0, 4 and 8 h incubation with scramble, shRNA for Mettl3 or Mettl14, mESC cells were collected and RNAs were isolated for microarray analysis using Affymetrix Genechip Mouse Gene 2.0 ST array. After 0 h incubation with scramble, shRNA for Mettl3 or Mettl14, mESC cells were collected and RNAs were isolated for microarray analysis using Affymetrix Genechip Mouse Gene 2.0 ST array.
Project description:To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates
Project description:Insulin binds the insulin receptor (IR), which in turn has showed to form nanoclusters at the cell membrane. Trying to exploit the nanoscale spatial organization of IR, we developed rod-like insulin-DNA-origami nanostructures carrying different numbers of insulin molecules. These structures (referred to as NanoRods, or NR) were then utilized to investigate receptor activity to spatial distribution of insulin molecules. One part of this investigation was to study the transcriptional response of brown adipocytes treated with NR bound to one insulin (NR-1) and NR bound to seven insulin (NR-7), and compare to untreated controls. Furthermore, free insulin was also used to ensure that similar pathways were activated when using NR-bound insulin.
Project description:Tau (MAPT) is a microtubule-associated protein causing frequent neurodegenerative diseases or inherited frontotemporal lobar degenerations. Emerging evidence for non-canonical functions of Tau in DNA protection and P53 regulation suggests its involvement in cancer. Indeed, Tau expression correlates with cancer-specific survival or response to microtubule therapeutics. These data may imply common molecular pathways involved in the pathogenesis of neurodegenerative disorders and cancer. To bring new evidence that Tau represents a key protein in cancer, we present an in silico pan-cancer analysis of MAPT transcriptomic profile in over 11000 clinical samples and over 1300 pre-clinical samples provided by the TCGA and the DEPMAP datasets respectively. We completed this analysis by exploring a possible interplay of MAPT with wild-type or mutated P53. Then, we calculated the impact of MAPT expression on clinical outcome and drug response. Overall, the results support a relevant role of the MAPT gene in several cancer types, although the contribution of Tau to cancer appears to very much depend on the cellular context.
Project description:The goal of the study was to investigate the effect of inducible ZXDA expression in HCT116 cell line. HCT116 clones expressing inducible versions of human ZXDA gene (2 clones wild-type; 2 clones ERP386-388AAA) were incubated with or without doxycycline.
Project description:During cancer progression, carcinoma cells encounter a variety of cytotoxic stresses such as hypoxia, nutrient deprivation, and low pH as a result of inadequate vascularization. To maintain survival and growth in the face of these physiologic stressors, a set of adaptive response pathways are induced. One adaptive pathway well studied in other contexts is the unfolded protein response (UPR), of which XBP1 is an important component. We used microarrays to detect transcriptome profile changes after XBP1 knockdown in breast cancer cell lines, and identify genes and pathways regulated by XBP1, which could help elucidate how XBP1 mediates the adaptive response of breast cancer to cytotoxic stresses. We extracted RNA and hybridized it to Affymetrix microarrays in two breast cancer cell lines (T47D and MDA-MB-231) under treated (hypoxia and glucose deprivation) or untreated conditions with XBP1 knockdown or not.