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

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

PROVIDER: PRJNA786567 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17150700_1.fastq.gz	Fastqsanger.gz
	SRR17150700_2.fastq.gz	Fastqsanger.gz
	SRR17150701_1.fastq.gz	Fastqsanger.gz
	SRR17150701_2.fastq.gz	Fastqsanger.gz
	SRR17150702_1.fastq.gz	Fastqsanger.gz

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MEK inhibition overcomes chemoimmunotherapy resistance by inducing CXCL10 in cancer cells

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

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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]

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

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

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.

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

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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

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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.

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

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Combined CDK inhibition overcomes MEK inhibitor resistance in plexiform neurofibroma of neurofibromatosis type I

Project description:Combined CDK inhibition overcomes MEK inhibitor resistance in plexiform neurofibroma of neurofibromatosis type I

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