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Exercise inhibits tumor progression and improves the therapeutic efficacy of PD-1 blockade in colorectal cancer preclinical models

ABSTRACT: Exercise inhibits tumor progression and improves the therapeutic efficacy of PD-1 blockade in colorectal cancer preclinical models

PROVIDER: PRJNA722267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14244176.fastq.gz	Fastqsanger.gz
	SRR14244177.fastq.gz	Fastqsanger.gz
	SRR14244178.fastq.gz	Fastqsanger.gz
	SRR14244179.fastq.gz	Fastqsanger.gz
	SRR14244180.fastq.gz	Fastqsanger.gz

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Exercise inhibits tumor progression and improves the therapeutic efficacy of PD-1 blockade in colorectal cancer preclinical models

Project description:Exercise training (ExT) has shown antitumor effects in many preclinical cancer models. In the present study, we utilize MC38 and CT26 cells, which represent MSI and MSS colorectal carcinomas respectively, to study the effects and mechanisms of ExT alone or in combination with PD-1 based immunotherapy. Using treadmill running and PD-1/PD-L1 blockade, we demonstrated that post-implant exercise training has broad anticancer activities in murine models of CRC. Specifically, in MSI CRC models, ExT induces beneficial metabolic and immunological adaptations, leading to a more significant inhibition in tumors treated with PD-1/PD-L1 blockade, suggesting a genotype-directed combinatory therapy for the subgroup of CRC patients. Moreover, ExT might be a safe and alternative anticancer strategy for cancers resistant to the PD-1 based immunotherapy, such as patients with MSS CRC tumors.

2021-04-16 | GSE172162 | GEO

Targeting tumor-intrinsic N7-methylguanosine tRNA modification inhibits MDSC recruitment and improves anti-PD-1 efficacy

Project description:We found that PMN-MDSCs level is elevated in the advanced ICCs tissues and is positively associated with the METTL1 and m7G tRNA modification levels. We further showed that impaired m7G tRNA modification impedes the PMN-MDSCs infiltration and inhibits ICC progression. Mechanistically, METTL1-mediated m7G tRNA modification selectively regulates the translation of human CXCL8 and mouse Cxcl5 transcripts, which facilitates the migration of PMN-MDSCs via binding to their cognate receptor CXCR2. Co-blockade of METTL1 and CXCR2 significantly enhances the efficacy of anti-PD-1 treatment in ICC. Taken together, our study reveals the cellular and molecular basis of crosstalk between ICC cells and MDSCs in shaping TIME and affecting ICIs efficacy, which enables reasonable design of new combined therapy targeting dysregulated mRNA translation and suppressive TIME.

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Therapeutic efficacy of FASN inhibition in preclinical models of HCC

Project description:Therapeutic efficacy of FASN inhibition in preclinical models of HCC

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Histone deacetylase inhibition replicates aspects of the adaptive response to exercise and improves muscle metabolism and cardiac function in obesity.

Project description:Drugs used to treat obesity and type 2 diabetes have limited efficacy in directly normalising muscle metabolism. The discovery of molecules mediating exercise adaptations, and drugs that modulate their activity, is a potential strategy to address this therapeutic gap. Here we show that genetic impairment of HDAC4 and 5 in mice regulated a subset of exercise responsive genes involved in metabolism and increased cell autonomous energy expenditure. Screening of HDAC inhibitors identified Scriptaid as a compound that also replicated aspects of the exercise adaptive response in vitro and in vivo. Treatment of obese mice with Scriptaid increased exercise performance, restored muscle insulin sensitivity and reduced muscle lipids. Scriptaid also increased oxygen consumption and normalised cardiac structure and function in obese mice. These data show that HDAC inhibition replicates aspects of the exercise adaptive response and that pharmacological HDAC inhibition could deliver more efficacious treatment to combat the metabolic diseases. Four-condition experiment, Empty, HDACs, Vehicle and Script-HDACs with five biological replicates for each condition. One replicate per array.

2015-01-28 | E-GEOD-54642 | biostudies-arrayexpress

Preclinical efficacy of the MTH1 inhibitor karonudib in B-cell lymphoma

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TNF blockade uncouples toxicity and anti-tumor efficacy induced with an agonist CD40 antibody

Project description:TNF mechanistically links cytokine release and hepatotoxicity triggered by an agonist CD40 antibody, and toxicity can be suppressed by blockade of TNF without affecting anti-tumor efficacy.

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Therapeutic efficacy of FASN inhibition in preclinical models of HCC

Project description:Background & Aims: Aberrant activation of fatty acid synthase (FASN) is a major metabolic event during the development of HCC. We evaluated the therapeutic efficacy of TVB3664, a novel FASN inhibitor, either alone or in combination, for HCC treatment. Approach & Results: The therapeutic efficacy and the molecular pathways targeted by TVB3664, either alone or with tyrosine kinase inhibitors or the checkpoint inhibitor anti-PD-L1 antibody, were assessed in human HCC cell lines and multiple oncogene-driven HCC mouse models. RNAseq was performed to characterize the global gene expression and metabolic profiles. TVB3664 effectively ameliorated the fatty liver phenotype in the aged mice and AKT activation-induced hepatic steatosis. TVB3664 monotherapy showed moderate efficacy in NASH-related murine HCCs, induced by loss of PTEN and c-MET overexpression. TVB3664, in combination with cabozantinib, triggered tumor regression in this mouse HCC model but did not improve the responsiveness to immunotherapy. Global gene expression revealed that TVB3664 predominantly modulated metabolic processes, while TVB3664 synergized with cabozantinib to downregulate multiple cancer-related pathways, especially the AKT/mTOR pathway and cell proliferation genes. TVB3664 also improved the therapeutic efficacy of sorafenib and cabozantinib in the FASN-dependent c-MYC HCC model. However, TVB3664 had no efficacy nor synergistic effects in FASN-independent mouse HCC models. Conclusions: This preclinical study suggests the limited efficacy of targeting FASN as monotherapy for HCC treatment. However, FASN inhibitors could be combined with other drugs for improved effectiveness. These combination therapies could be developed based on the driver oncogenes, supporting precision medicine approaches for HCC treatment.

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Histamine footprint on the human exercise transcriptome

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Histone deacetylase inhibition replicates aspects of the adaptive response to exercise and improves muscle metabolism and cardiac function in obesity.

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Exercise-acclimated microbiota improves skeletal muscle metabolism

Project description:Habitual exercise modulates the composition of the intestinal microbiota. We examined whether transplanting fecal microbiota from trained mice improved skeletal muscle metabolism in high-fat diet-fed mice. The recipient mice that received fecal samples from trained donor mice for 1 week showed elevated levels of metabolic signalings in skeletal muscle. Glucose tolerance was improved by fecal microbiota transplantation after 8 weeks of HFD administration. Intestinal microbiota may mediate exercise-induced metabolic improvement in mice. We performed a microarray analysis to compare the metabolic gene expression profiles in the skeletal muscle from each mouse.

2022-06-30 | GSE201202 | GEO

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