Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting MUC1-C sensitizes colorectal cancer cells to BRAF inhibitor

ABSTRACT: Targeting MUC1-C sensitizes colorectal cancer cells to BRAF inhibitor

PROVIDER: PRJNA890903 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21918700_1.fastq.gz	Fastqsanger.gz
	SRR21918700_2.fastq.gz	Fastqsanger.gz
	SRR21918701_1.fastq.gz	Fastqsanger.gz
	SRR21918701_2.fastq.gz	Fastqsanger.gz
	SRR21918702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Targeting MUC1-C sensitizes colorectal cancer cells to BRAF inhibitor

Project description:BRAF mutant colorectal cancer has a poor prognosis and gets resistant to BRAF inhibitors quickly. This study aims to clarify the mechanism of resistance to BRAFi. We found MCU1-C is overexpressed in BRAF mutant colorectal cancer and targeting MUC1-C genetically and pharmacologically sensitized Colorectal cancer cells to BRAF inhibitor. This finding suggests that MUC1-C could be a new therapeutic target for BRAF mutant colorectal cancer.

2022-11-30 | GSE215849 | GEO

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

BRAF paradox breakers PLX8394 and PLX7904 comparison to BRAF inhibitor PLX4720 effect on BRAF V600Ε mutant colorectal adenocarcinoma cells

Project description:BRAF paradox breakers PLX8394 and PLX7904 comparison to BRAF inhibitor PLX4720 effect on BRAF V600Ε mutant colorectal adenocarcinoma cells

| PRJEB38086 | ENA

Expression of BRAF inhibitor resistant colon cancer lines

Project description:Colon cancer cell lines with partial sensitivity to the BRAF inhibitor PLX4720 were grown in increasing concentration of the drug to develop acquired resistance. Gene expression was performed for comparison of the resistant clones to the parental lines. Colon cancer cell lines with partial sensitivity to the BRAF inhibitor PLX4720 were grown in increasing concentration of the drug to develop acquired resistance. Gene expression was performed for comparison of the resistant clones to the parental lines.

2012-09-15 | E-GEOD-34299 | biostudies-arrayexpress

Targeting PLK1-CBX8-GPX4 axis overcomes BRAF/EGFR inhibitor resistance in BRAFV600E colorectal cancer via ferroptosis

Project description:Metastatic BRAFV600E colorectal cancer (CRC) confers poor prognosis and represents a therapeutic bottleneck. To identify resistance mechanisms of the mitogen-activated protein kinase (MAPK) pathway in BRAFV600E CRC, we perform genome-wide CRISPR-Cas9 screening and discover that targeting glutathione peroxidase 4 (GPX4) overcomes resistance to BRAF inhibitor (BRAFi) combined with or without epidermal growth factor receptor inhibitor (EGFRi) in BRAFV600E CRC. Specifically, BRAFi ± EGFRi upregulates GPX4 expression, which antagonizes therapy-induced ferroptosis. Moreover, polo-like kinase 1 (PLK1) substrate activation promotes PLK1 translocation to the nucleus, activating chromobox protein homolog 8 (CBX8) phosphorylation at Ser265 to drives GPX4 expression. Targeting PLK1 enhances BRAFi ± EGFRi inhibition and triggers ferroptosis in vitro, vivo, organoid, and patient-derived xenograft model. Collectively, we demonstrate a PLK1–CBX8–GPX4 signaling axis that relays the ferroptosis mechanism of therapeutic resistance and propose a clinically actionable strategy to overcome BRAFi ± EGFRi resistance in BRAFV600E CRC.

2025-02-28 | GSE283185 | GEO

Epigenetic reprogramming in adaptive drug resistance to BRAF inhibitor therapy

Project description:The development of drug resistance is a major limiting factor to the efficacy of BRAF inhibitor therapy for melanoma. The goal of this study was to identify and characterize pathways that contribute to adaptive drug resistance to BRAF inhibitors.

2021-12-31 | GSE156302 | GEO

MUC1-C is necessary for SHP2 activation and BRAF inhibitor resistance in BRAF(V600E) mutant colorectal cancer.

Project description:Colorectal cancers (CRCs) harboring the BRAF(V600E) mutation are associated with aggressive disease and resistance to BRAF inhibitors by feedback activation of the receptor tyrosine kinase (RTK)→RAS→MAPK pathway. The oncogenic MUC1-C protein promotes progression of colitis to CRC; whereas there is no known involvement of MUC1-C in BRAF(V600E) CRCs. The present work demonstrates that MUC1 expression is significantly upregulated in BRAF(V600E) vs wild-type CRCs. We show that BRAF(V600E) CRC cells are dependent on MUC1-C for proliferation and BRAF inhibitor (BRAFi) resistance. Mechanistically, MUC1-C integrates induction of MYC in driving cell cycle progression with activation of the SHP2 phosphotyrosine phosphatase, which enhances RTK-mediated RAS→ERK signaling. We demonstrate that targeting MUC1-C genetically and pharmacologically suppresses (i) activation of MYC, (ii) induction of the NOTCH1 stemness factor, and (iii) the capacity for self-renewal. We also show that MUC1-C associates with SHP2 and is required for SHP2 activation in driving BRAFi-induced feedback of ERK signaling. In this way, targeting MUC1-C in BRAFi-resistant BRAF(V600E) CRC tumors inhibits growth and sensitizes to BRAF inhibition. These findings demonstrate that MUC1-C is a target for the treatment of BRAF(V600E) CRCs and for reversing their resistance to BRAF inhibitors by suppressing the feedback MAPK pathway.

| S-EPMC10408991 | biostudies-literature

Transcriptomic profiling of melanomas treated with BRAF inhibitor

Project description:Transcriptomic profiling of melanomas treated with BRAF inhibitor

| PRJNA678300 | ENA

Expression data of BRAF inhibitor resistant melanoma cells

Project description:Expression data of BRAF inhibitor resistant melanoma cells

| PRJNA471347 | ENA

protein levels in BRAF inhibitor resistance melanoma cells treated with PF3758309

Project description:11 BRAF inhibitor resistance melanoma cells were treated with PAK inhibitor PF3758309 for 48 hr, the cell lysis were analyzed by RPPA profiling by protein array (RPPA)

2017-07-31 | GSE96753 | 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