Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1018107 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Label-free whole cell proteomics was performed for the following cell lines: LHS-PREC engineered to overexpress MYC or EV; P4936 overexpressing MYC on a tetracycline-repressible promotor; MCF10A cells expressing signal transduction oncogenes AKT, BRAF, EGFR, HER2, KRAS, MEK; KP4 and PSN1 PDAC cell lines vs HPDE normal pancreatic cell; PDX-derived osteosarcoma cell lines with MYC amplification vs hFOB cell
2022-08-11 | PXD033373 | Pride
Project description:Effect of STN1 knockdown on gene expression of PDAC cell lines
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Project description:In our experiments, we showed that FAK regulates PDAC clonogenicity and selfrenewal. In order to evaluate the impact of FAK knockdown on the transcriptomes of PDAC , we knocked down FAK in two PDAC cell lines and compared the gene expression signatures with the cancer stem cell (CSC)associated gene signatures by GSEA analysis. CCS related gene profile was inversely related with FAK-knockdown gene signature.
2017-04-20 | GSE97488 | GEO
Project description:Understanding the molecular mechanisms underlying tumorigenesis is crucial for developing effective cancer therapies. Here, we investigate the common co-amplification of MED30 and MYC across diverse cancer types and its impact on oncogenic transcriptional programs. Transcriptional profiling of MYC and MED30 single or both overexpression/amplification revealed the over amount of MED30 lead MYC to a new transcriptional program that associate with poor prognosis. Mechanistically, MED30 overexpression/amplification recruits other Mediator components and binding of MYC to a small subset of novel genomic regulatory sites, changing the epigenetic marks and inducing the formation of new enhancers, which drive the expression of target genes crucial for cancer progression. In vivo studies in pancreatic ductal adenocarcinoma (PDAC) further validate the oncogenic potential of MED30, as its overexpression promotes tumor growth and can be attenuated by knockdown of MYC. Using another cancer type, MED30 knockdown reduces tumor growth particularly in MYC high-expressed glioblastoma (GBM) cell lines. Overall, our study elucidates the critical role of MED30 overexprssion in orchestrating oncogenic transcriptional programs and highlights its potential as a therapeutic target for MYC-amplified cancer.
2024-05-30 | GSE264275 | GEO
Project description:Array Comparative Genomic Hybridization (aCGH) of 70 pancreatic ductal adenocarcinoma (PDAC) samples was performed on Agilent 244K CGH arrays in order to find common genomic aberrations for cancer gene discovery. Additionally, matched expression profiling on Agilent 44K arrays was performed. Common copy number aberrations were identified in order to identify a list of putative cancer genes. Expression profiling data was used to further enrich this list of putative cancer genes for more likely candidates. Last, the most promising candidates were functionally interrogated using RNA interference-mediated knockdown to mimic loss. Well-known PDAC cancer genes were observed as amplified (KRAS and MYC) and deleted (CDKN2A, TGFBR2, SMAD4, and MAP2K4). 70 tumor samples (48 xenografts, 22 cell lines). 2-color arrays hybridized against a common reference pool of genomic DNA from 8 normal individuals. This dataset represents the aCGH component of the study.
2011-12-15 | E-GEOD-25273 | biostudies-arrayexpress
Project description:C-Myc overexpression is an important molecular hallmark of pancreatic ductal adenocarcinoma (PDAC), but directly targeting c-Myc is extremely challenging. Identifying key upstream factors involved in c-Myc overexpression provides promising indirect targets for c-Myc. Herein, the long noncoding RNAs (lncRNAs) highly expressed in PDAC and significantly correlated with c-Myc expression were identified using RNA sequencing datasets. Among them, LINC01963 was found to interact with c-Myc, as confirmed by RNA pull-down and RIP-qPCR assays. Furthermore, high LINC01963 expression was correlated with poor PDAC prognosis, and functional studies demonstrated that its knockdown inhibited PDAC cell proliferation and xenograft tumor growth. Mechanistic studies identified LINC01963 as a key regulator of c-Myc stability, consequently affecting cell cycle through the c-Myc/p21-related signaling pathways. Further investigation revealed that LINC01963 enhanced N6-methyladenosine (m6A) modification of c-Myc mRNA by protecting methyltransferase-like 3 (METTL3) protein from KDM1B-mediated ubiquitin-proteasome degradation. Intriguingly, LINC01963 also stabilized c-Myc mRNA by facilitating the formation of a ternary complex with insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and m6A-modified c-Myc. Our study reveals that LINC01963 promotes PDAC tumorigenesis through METTL3/IGF2BP2 axis-coordinated regulation of c-Myc, suggesting a new strategy for indirectly targeting c-Myc.
2025-04-29 | GSE295171 | GEO
Project description:Lentivirus carrying shRNAs targeting MLL4 was transduced into CAPAN2 and PANC1 cells. Gene expression affected by the knockdown of MLL4 in PDAC cell lines will be revealed.
2020-05-31 | E-MTAB-9073 | biostudies-arrayexpress
Project description:The dolichyl-diphosphooligosaccharide-protein glycosyltransferase non-catalytic subunit (DDOST) is a key component of the oligosaccharyltransferase complex catalyzing N-linked glycosylation in the endoplasmic reticulum lumen. DDOST is associated with several cancers and congenital disorders of glycosylation. However, its role in pancreatic cancer remains elusive, despite its enriched pancreatic expression. Using quantitative mass spectrometry, we identify 30 differentially expressed proteins and phosphopeptides (DEPs) after DDOST knockdown in the pancreatic ductal adenocarcinoma (PDAC) cell line PA-TU-8988T. We evaluated DDOST / DEP protein-protein interaction networks using STRING database, correlation of mRNA levels in pancreatic cancer TCGA data, and biological processes annotated to DEPs in Gene Ontology database. The inferred DDOST regulated phenotypes were experimentally verified in two PDAC cell lines, PA-TU-8988T and BXPC-3. We found decreased proliferation and cell viability after DDOST knockdown, whereas ER-stress, ROS-formation and apoptosis were increased. In conclusion, our results support an oncogenic role of DDOST in PDAC by intercepting cell stress events and thereby reducing apoptosis. As such, DDOST might be a potential biomarker and therapeutic target for PDAC.
2024-09-03 | PXD047441 | Pride
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