Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA513104 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional sequencing of IGF2BP2-knockdown and control group of human PDAC cell line BxPC-3
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Project description:Transcriptome of human pancreatic ductal adenocarcinoma cell line with IGF2BP2 knockdown and control group
| PRJNA510864 | ENA
Project description:Transcriptome of human pancreatic ductal adenocarcinoma cell line with IGF2BP2 knockdown and control group
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Project description:Characterization of the protein composition of exosomes and subpopulations of cells from four human PDAC cell lines (BxPC-3, PANC-1, T3M4, and MIA PaCa-2), via liquid chromatography electrospray ionization tandem mass spectrometry (LC/ESI–MS/MS).
2022-01-25 | PXD023529 | Pride
Project description:We report that m6A reader IGF2BP2 participates in the regulation of glutamine metabolism in AML. To further clarify whether IGF2BP2 knockdown (KD) leads to translational inhibition, we perform Ribo-seq in control and IGF2BP2 KD cells.
2022-11-01 | GSE211618 | GEO
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignant leukemia with extreme limited treatment for relapsed patients. N6‐methyladenosine (m6A) reader Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) participates in the initiation and growth of cancers by communicating with various targets. Here, we found IGF2BP2 is highly expressed in T-ALL. Gain and loss of IGF2BP2 demonstrated IGF2BP2 was essential for T-ALL cell proliferation in vitro and loss of IGF2BP2 prolonged animal survival in a human T-ALL xenograft model. Mechanistically, IGF2BP2 directly bound to T-ALL oncogene NOTCH1 via an m6A dependent manner. Furthermore, we identified a small-molecule IGF2BP2 inhibitor JX5 and treatment of T-ALL with JX5 showed similar functions as knockdown of IGF2BP2. These findings not only shed light on the role of IGF2BP2 in T-ALL, but also provide an alternative γ‑Secretase inhibitors (GSI) therapy to treat T-ALL.
2022-07-04 | GSE207323 | GEO
Project description:Purpose: Due to its high metastatic proclivity, pancreatic ductal adenocarcinoma (PDAC) is one of the most deadly types of cancer. Therefore, it is imperative to better understand how the disease spreads as it progresses. Using a novel genetically engineered mouse model that allows us to isolate a subpopulation of cancer cells with superior metastatic capacity, we show that this aggressive phenotype correlates exclusively with a strong hypoxia signature. We subsequently identified the novel hypoxia-inducible gene Blimp1, which appears to play a critical role in regulating the hypoxic response upon its induction. Furthermore, genetic ablation of Blimp1 greatly reduces the level of metastasis in a PDAC mouse model. The nature of this Blimp1-regulated hypoxia signature is very unstable, since the seeded metastatic lesions mostly re-adopt similar transcriptomic profiles as the primary tumors. In conclusion, our results offer a potential mechanistic insight into how hypoxia drives metastasis in PDAC. Methods: The liver metastasis cell line 688M was subjected to control or knockdown of Blimp1 before assay. Cells ere validated for knockdown efficiency and then cultured under normoxia and hypoxia (0.5% O2) for 24 hours before preparation for ATAC-Seq (total of 4 groups with 2 technical replicates per group, overall 8 samples). Reference for ATACSeq: Buenrostro et al. 2013. Nat Methods 12:1213-8. Results: For the control knockdown group, 0.5% O2 culture (hypoxia) for 24 hours induced dramatic changes in global genome accessibility, and Blimp1 knockdown appeared to induce minimum changes in chromatin accessibility under hypoxia or normoxia (20% O2). Conclusions: Compared to our RNASeq profiles of the same liver met PDAC cell line under identical conditions, Blimp1 appeared to impact a global gene expression changes under hypoxia that is not associated with a corresponding changes of chromatin accessibility.
2017-08-01 | GSE90918 | GEO
Project description:This microarray is an analysis of differentially expressed genes in three pancreatic ductal adenocarcinoma cell lines treated with LXR-agonist GW 3965. We first report that GW 3965 has antiproliferative effects in three PDAC cell lines. This microarray was designed to identify key mechanisms of the antiproliferative effect of LXR agonists within pancreatic cancer cell lines. Total RNA obtained from BxPC-3, MIA-PaCa-2, and PANC-1 pancreatic cancer cells grown in culture treated GW 3965 or ethanol (vehicle control) for 72 hours.
2014-04-15 | E-GEOD-51656 | biostudies-arrayexpress
Project description:The goal of this study was to determine IGF2BP3 regulation of RNA targets in human pacreatic ductal adenocarcinoma cell lines Included are iCLIP-seq libraries for IGF2BP3 from PL45 and Panc1 PDAC cell samples, RIP-seq samples from PL45 and Panc1 PDAC cells, RNA-seq data sets from control and IGF2BP3 knockdown in PL45 and Panc1 PDAC cells, and small RNA-seq samples from Panc1 cells
2016-03-12 | E-GEOD-79147 | biostudies-arrayexpress
Project description:Protein arginine methylation has been established an essential protein modification regulating cancer initiation and progression, but its implications in PDAC (Pancreatic ductal adenocarcinoma) still remains poorly elucidated. In this study, we characterized ADMA (asymmetric dimethylarginine)-bearing peptides in human pancreatic ductal epithelium cell line HPDE6c7 and PDAC cell line PANC-1 by a label-free quantitative proteomics combined with affinity purification.
2020-02-18 | PXD017577 | iProX