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MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [LLC1]

ABSTRACT: MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [LLC1]

PROVIDER: PRJNA786566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17150673.fastq.gz	Fastqsanger.gz
	SRR17150674.fastq.gz	Fastqsanger.gz
	SRR17150675.fastq.gz	Fastqsanger.gz
	SRR17150676.fastq.gz	Fastqsanger.gz
	SRR17150677.fastq.gz	Fastqsanger.gz

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MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [LLC1]

Project description:Chemotherapy with anti PD-1/PD-L1 mAb has become the standard of care for patients with metastatic non-small cell lung cancer (NSCLC). Using lung tumor models, where pemetrexed-platinum chemotherapy (PEM/CDDP) remains unable to synergize with immune checkpoint inhibitors (ICI), we linked failure of this treatment with its inability to induce CXCL10 expression and CD8+ T cell recruitment. Using drug screening, we showed that combining a MEK inhibitor (MEKi) with PEM/CDDP triggers CXCL10 secretion by cancer cells and CD8+ T cell recruitment, and restores ICI efficacy. PEM/CDDP plus MEKi promotes optineurin (OPTN)-dependent mitophagy, resulting in CXCL10 production in a mitochondrial DNA and TLR9-dependent manner. TLR9 or autophagy/mitophagy processes genetic inactivation of abort the antitumor efficacy of PEM/CDDP plus MEKi/anti PD-L1 therapy. In human NSCLC, high OPTN, TLR9 and CXCL10 expression is associated with better response to ICI. Our results underline the role of TLR9 and OPTN-dependent mitophagy in enhancing chemoimmunotherapy efficacy.

2021-12-08 | GSE190264 | GEO

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells

Project description:MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells

| PRJNA786564 | ENA

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France4]

Project description:MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France4]

| PRJNA786567 | ENA

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France3]

Project description:MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France3]

| PRJNA786565 | ENA

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France4]

2021-12-08 | GSE190266 | GEO

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells [France3]

2021-12-08 | GSE190265 | GEO

MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-08 | GSE190270 | GEO

Targeting β-catenin overcomes resistance to MEK inhibitor in PIK3CA mutant colon cancer

Project description:Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identified a gene that cooperates with MEK inhibitors to forcefully treat PIK3CA mutant colon cancer cells. -catenin, a key molecule of the WNT pathway, emerged as a candidate by protein/Ab Chip array. MEK inhibitor treatment led to a decrease in -catenin in PIK3CA wild-type colon cancer cells but not in PIK3CA mutant colon cancer cells. Tumor regression was promoted by a combination of MEK inhibitor and NVP-TNS656, which targets the WNT pathway. Furthermore, combined inhibition of MEK and -catenin by NVP-TNS656 promoted tumor regression in colon cancer patient-derived xenograft (PDX) models expressing mutant PIK3CA. Taken together, we propose that inhibition of the WNT pathway, particularly -catenin, may bypass resistance to MEK inhibitor in human PIK3CA mutant colon cancer. Additionally, -catenin is a potential PD marker of MEK inhibitor resistance. In the study, we identified and evaluated biomarker for response to MEK inhibitor on colon cancer cells.

2015-08-13 | E-GEOD-71981 | biostudies-arrayexpress

Analysis by Whole Transcriptome Sequencing of the Effects of LLC1 conditioned medium, LLC1 conditioned plus Calcitriol, non-conditioned medium, and non-conditioned medium plus Calcitriol on mRNA Expression in Primary Human Skeletal Muscle Cells

Project description:Primary human skeletal muscle cells (Lonza) were treated with LLC1 conditioned medium, LLC1 conditioned medium plus Calcitriol, LLC1 non-conditioned medium or LLC1 non-conditioned medium plus Calcitriol for a period of 24 hours prior to isolation of RNA.

2018-02-07 | GSE103549 | GEO

Targeting β-catenin overcomes resistance to MEK inhibitor in PIK3CA mutant colon cancer

2015-08-13 | GSE71981 | GEO