Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975-RT_vs_H1975-OR]

ABSTRACT: MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975-RT_vs_H1975-OR]

PROVIDER: PRJNA1129173 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR29633216_1.fastq.gz	Fastqsanger.gz
	SRR29633216_2.fastq.gz	Fastqsanger.gz
	SRR29633217_1.fastq.gz	Fastqsanger.gz
	SRR29633217_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975-RT_vs_H1975-OR]

Project description:MUC1-C is necessary for establishing and recalling resistance of NSCLC cells to osimertinib by driving an inflammatory memory responseThe oncogenic MUC1-C protein functions as a master regulator of NSCLC cell resistance to osimertinib by unclear mechanisms. We report that MUC1-C-mediated regulation of STAT1 and the interferon (IFN) type I/II pathways is necessary for establishing osimertinib resistance. Studies of osimertinib-resistant NSCLC cells selected for growth in the absence of drug further demonstrate that revertant cells are dependent on MUC1-C for recalling resistance to osimertinib. We show that establishing and recalling osimertinib resistance is dependent on activation of the MUC1 gene at (i) a proximal enhancer-like signature 1 (pELS-1) by MUC1-C and STAT1 and (ii) a pELS-2 by MUC1-C, JUN/AP-1 and PBAF. The MUC1 pELS regions function as memory domains for activation of MUC1-C and downstream STAT1 and IFN stimulated genes in conferring osimertinib resistance. Of clinical relevance, we report that the MUC1-C-driven inflammatory responses are induced in patient-derived, osimertinib-resistant MGH170 NSCLC cells with MET amplification. Our results further demonstrate that MGH170 cells are dependent on the MUC1-C-induced inflammatory response for resistance to the osimertinib and combination of osimertinib with the MET inhibitor capmatinib. These findings indicate that MUC1-C is necessary for establishing and recalling resistance of NSCLC cells to osimertinib by driving an inflammatory memory response.

2025-06-26 | GSE270997 | GEO

MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975_vs_H1975-OR]

2025-06-26 | GSE270995 | GEO

Muc1-C Regulates Neat1 Lncrna Expresmuc1-C Is Essential For Establishing And Recalling Inflammatory Memory Of Osimertinib Resistance In Nsclc Cellssion And Paraspeckle Formation In Cancer Stem Cells

2025-04-02 | GSE263757 | GEO

MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975_vs_H1975-OR]

Project description:MUC1-C IS ESSENTIAL FOR ESTABLISHING AND RECALLING INFLAMMATORY MEMORY OF OSIMERTINIB RESISTANCE IN NSCLC CELLS [H1975_vs_H1975-OR]

| PRJNA1129175 | ENA

Osimertinib resistant cells of H1975

Project description:Osimertinib resistant cells of H1975

| PRJNA767314 | ENA

MUC1-C IS ESSENTIAL FOR INFLAMMATORY MEMORY OF TYROSINE KINASE INHIBITOR RESISTANCE IN NSCLC CELLS

Project description:This study identifies the oncogenic protein MUC1-C as a key driver of resistance to the EGFR tyrosine kinase inhibitor osimertinib in non-small cell lung cancers (NSCLCs).MUC1-C promotes resistance by activating STAT1 and type I/II interferon pathways, creating an inflammatory memory of the resistant phenotype. This memory is maintained via MUC1-C/STAT1 interaction at one enhancer region (pELS-1) and MUC1-C/JUN/PBAF at another (pELS-2) in the MUC1 gene. MUC1-C also mediates resistance to combination EGFR/MET inhibitors and a fourth-generation EGFR TKI (TQB3804). Importantly, targeting MUC1-C with an antibody-drug conjugate (M1C ADC) is effective both in vitro and in a patient-derived xenograft model, making MUC1-C a promising therapeutic target for TKI-refractory NSCLC.

2025-04-22 | GSE294981 | GEO

Disclosing potential therapeutic targets associated with Osimertinib resistance in non-small cell lung cancer cell line H1975

Project description:Osimertinib, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor, is a highly effective and valuable treatment option for advanced non-small cell lung cancer (NSCLC) patients with EGFR mutations, like T790M. However, acquired resistance ultimately limits its clinical application. In this study, we constructed H1975/OSI cell lines and utilized potentially complementary transcriptomic and proteomic techniques, which may provide insight into the intricately complex molecular mechanisms, to reveal potential therapeutic targets associated with Osimertinib resistance. Uni-omics and multi-omics analyses were conducted on the transcriptomic and proteomic (4D label-free) expression profiles, which involved differential expression analysis, GO functional annotation and KEGG pathway enrichment analysis, correlation analysis of transcription factors, PPI network and Cytoscape analysis. We highlighted multiple signaling pathways and eleven hub-genes, including NOP56, DDX21, PDCD11, CCNB1, TOP21, KPNA2, DDX5, EFTUD2, BRCA1, LMNB1 and HIF1A, that may be the key to overcoming resistance. Further validation of these targets and molecules in preclinical and clinical studies could lead to the development of new and more effective treatment options for H1975-resistant patients.

2024-08-05 | GSE236654 | GEO

Expression data of osimertinib tolerant H1975 cells

Project description:Expression data of osimertinib tolerant H1975 cells

| PRJNA827146 | ENA

Gene expression data in the human non-small cell lung cancer cell line NCI-H1975 and osimertinib-resistant OR1 and OR2 cells

Project description:Osimertinib, a third-generation EGFR-TKI, has applied to non-small cell lung cancer harboring activated EGFR mutation with or without T790M. However, the appearance of tumors resistant to osimertinib has been reported. We established and characterized osimertinib-resistant cells derived from NCI-H1975 cells harboring activating EGFR and T790M mutation.

2022-04-28 | GSE201608 | GEO

CircSPINT2 Confers Sensitivity to Osimertinib via hsa-miR-1296-3p/RBP1 Axis and Inhibits NSCLC Progression

Project description:Lung adenocarcinoma (LUAD) is the most common type of lung cancer. Resistance to osimertinib, a 3rd generation EGFR-TKI, develops within 12 months in patients with EGFR T790M mutation. This study used RNA-seq to identify circular RNAs (circRNAs) regulating osimertinib resistance in LUAD. We identified circSPINT2 as downregulated in osimertinib-resistant cell lines (OR3, OR4, OR6, HOsR) compared to parental H1975 cells. circSPINT2 enhances osimertinib sensitivity by inducing apoptosis via the hsa-miR-1296-3p/RBP1 axis. circSPINT2 is proposed as a non-invasive biomarker for monitoring osimertinib resistance in LUAD.

2025-11-14 | GSE295915 | 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