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

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

PROVIDER: PRJNA1252146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33198141_1.fastq.gz	Fastqsanger.gz
	SRR33198141_2.fastq.gz	Fastqsanger.gz
	SRR33198142_1.fastq.gz	Fastqsanger.gz
	SRR33198142_2.fastq.gz	Fastqsanger.gz
	SRR33198143_1.fastq.gz	Fastqsanger.gz

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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.

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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 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.

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

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