Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

ABSTRACT: We identify a collection of candidate lncRNAs interacted with c-Myc in pancreatic cancer and show for the first time that an lncRNA among them, which is named as c-Myc-stabilizing and activating RNA (MSAR), promotes pancreatic cancer proliferation and metastasis through c-Myc. MSAR enhances the interaction of c-Myc and SNIP1. These findings shed light on the pro-tumorigenic role of MSAR and might provide a novel therapeutic strategy for indirect targeting c-Myc in PDAC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181777 | GEO | 2023/09/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ZDHHC20-Mediated S-Palmitoylation of YTHDF3 Stabilizes MYC mRNA to Promote Pancreatic Cancer Progression

Project description:Post-translational modifications of malignant transformation and tumor maintenance in pancreatic ductal adenocarcinoma (PDAC) in the context of KRAS signaling remains largely unexplored. Here, we used the KPC mouse model to examine the effect of palmitoylation on pancreatic cancer progression. ZDHHC20, upregulated by KRAS, is abnormally overexpressed and associated with poor prognosis in patients with pancreatic cancer. Dysregulation of ZDHHC20 promotes pancreatic cancer progression in a palmitoylation-dependent manner. ZDHHC20 inhibits lysosomal localization and degradation of YTHDF3 through S-palmitoylation of Cys474, which can result in abnormal accumulation of the oncogenic product MYC and thereby promote the malignant phenotypes of cancer cells. Further, we designed a biologically active YTHDF3-derived peptide to competitively inhibit YTHDF3 palmitoylation mediated by ZDHHC20, which in turn downregulated MYC expression and inhibited the progression of KRAS mutant pancreatic cancer. Thus, these findings highlight the therapeutic potential of targeting the ZDHHC20-YTHDF3-MYC signaling axis in pancreatic cancer.

2024-04-22 | GSE235516 | GEO

LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

Project description:LncRNA MSAR stabilizes c-Myc to promote pancreatic cancer malignancy

| PRJNA753460 | ENA

Transcriptional co-factor Transducin beta-like (TBL) 1 acts as a checkpoint in pancreatic cancer malignancy

Project description:Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer fatalities in Western societies, characterized by high metastatic potential and resistance to chemotherapy. Critical molecular mechanisms of these phenotypical features still remain unknown, thus hampering the development of effective prognostic and therapeutic measures in PDAC. Here we show that transcriptional co-factor Transducin beta-like (TBL) 1 was over-expressed in both human and murine PDAC. Inactivation of TBL1 in human and mouse pancreatic cancer cells reduced cellular proliferation and enhanced chemosensitivity, correlating with diminished glucose uptake, glycolytic flux, and PI3kinase signaling. TBL1 deficiency both prevented and reversed pancreatic tumor growth in mice, triggering transcriptional PI3kinase inhibition also in vivo. As TBL1 mRNA levels were also found to correlate with overall and disease-free survival in a cohort of human PDAC patients and to predict therapy responsiveness in these subjects, TBL1 expression may serve both as a novel prognostic marker and molecular target in the treatment of human PDAC. Capan-1 cells were transfected with control-siRNA (#1027292, Qiagen) or siRNA against human TBL1 (SI04329514, Qiagen) and RNA was isolated 24h later

2015-06-16 | E-GEOD-59761 | biostudies-arrayexpress

RNA-seq of pancreatic CAF-derived cell line 0082T treated with Autotaxin inhibitors (IOA-289 and PF-8380) against DMSO treated controls

Project description:Autotaxin (ATX), encoded by ENPP2, catalyzes the production of lysophosphatidic acid (LPA), an important regulator within the tumor microenvironment (TME). ATX is a clinical target in pancreatic ductal adenocarcinoma (PDAC), yet the pro-tumorigenic action of the ATX/LPA axis in PDAC remains unclear. PDAC is characterized by a highly fibrotic tumor microenvironment (TME) due to an abundance of cancer associated fibroblasts (CAFs), acting as a barrier to therapy and contributing to the poor survival of PDAC patients. The mechanism by which ATX inhibition influences CAFs and their secretome is still not fully characterized. To identified potential downstream mediators of ATX signaling, we performed RNA-seq of pancreatic CAF-derived cell line 0082T treated with Autotaxin inhibitors, IOA-289 and PF-8380. PF-8380 treatment resulted in a higher number of differentially expressed genes compared to IOA-289 treatment. IOA-289 treatment resulted in only four significantly differentially expressed genes (CTGF, PLIN2, HHIP, and AHNAK). However, only PLIN2, which was upregulated and CTGF, which was downregulated, overlapped between the two ATX inhibitors. As CTGF (connective tissue growth factor) is a pro-fibrotic and pro-tumorigenic factor, it suggests a key role for CAF-derived ATX in promoting autocrine and paracrine pro-tumorigenic signaling in PDAC.

2024-10-06 | E-MTAB-14494 | biostudies-arrayexpress

LC-MS/MS analyses of human PDAC cell lines after treatment with a new SUMO inhibitor

Project description:Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with overall five-year survival of 8%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC, however subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumor biology. It is clear that hyperactivation of MYC generates dependencies that can be exploited therapeutically. To find MYC-associated dependencies we analyzed human PDAC expression datasets. We observed that MYC is connected to the SUMOylation machinery in PDAC. Components of the SUMO pathway mark a PDAC subtype with worse prognosis and we provide evidence that hyperactivation of MYC is connected to an increased sensitivity to a novel SUMO inhibitor with a potential for further clinical development.

2020-01-06 | PXD011347 | Pride

Transcriptional profiling of autophagy proficient and compromised cell lines, determined by expression levels of Atg5

Project description:Autophagy is activated in pancreatic ductal adenocarcinoma (PDAC) and is currently being considered a promising therapeutic target in clinical trials. PDAC is a highly lethal disease with incidence rate equalling mortality rate. Main reasons for PDAC lethality are late-stage diagnosis, high agressiveness and metastatic rate, lack of effective treatments as well as specific diagnostic markers. Here we show that varying levels of the Autophagy related gene 5 (Atg5) determine pancreatic tumor formation and malignancy. While homozygous deletion of Atg5 blocks tumor progression in an in vivo model of PDAC, heterozygous deletion increases tumor aggressiveness and metastasis. Further analyses reveal that monoallelic loss of Atg5 affects mitochondrial homeostasis, changes intracellular calcium oscillations, heightens extracellular cathepsin activities , and promotes a pro-tumorigenic inflammatory microenvironment collectively enhancing tumor cell migration, invasion, and metastasis. Future treatments should take into account that variations in the autophagy pathway may have opposing effects on pancreatic tumor load, especially considering the multitude of autophagy inhibitors currently tested in clinical trials.

2018-10-15 | E-MTAB-6275 | biostudies-arrayexpress

Transcriptional co-factor Transducin beta-like (TBL) 1 acts as a checkpoint in pancreatic cancer malignancy

2015-06-16 | GSE59761 | GEO

Label-free whole cell proteomics for oncogene cell lines

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

The SUMO Pathway as a Therapeutic Option in Pancreatic Cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with overall five-year survival of 8%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC, however subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumor biology. It is clear that hyperactivation of MYC generates dependencies, which can be exploited therapeutically. To find MYC-associated dependency we analyzed human PDAC expression dataset. We observed that MYC is connected to the sumoylation machinery in PDAC. Components of the SUMO pathway mark a PDAC subtype with worse prognosis and we provide evidence that PDACs with a MYChigh/SUMOhigh phenotype respond to a novel SUMO inhibitor, offering the opportunity to develop novel stratified PDAC therapies

2019-01-01 | GSE119423 | GEO

Identification of miR-29a-mediated target transcriptome in human pancreatic stellate cells (hPSCs) using RNAseq approach

Project description:In this study, we aim to understand the role of miR-29a in in regulating hPSCs. Identification of the differentially expressed direct and indirect miR-29a targets and the associated pathways from the RNASeq data delineates gene interactions and networks essential for activated PSCs in pancreatic ductal adenocarcinoma (PDAC) in regulating desmoplasia and tumor-stomal crosstalk, which are crucial mechanisms for PDAC progression.

2020-07-20 | GSE144767 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data