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MiR-24 induces human T cell exhaustion though mitochondria energy metabolic reprograming via suppressing MYC and FGF11

ABSTRACT: miR-24 induces human T cell exhaustion though mitochondria energy metabolic reprograming via suppressing MYC and FGF11

PROVIDER: PRJNA433927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6714660_1.fastq.gz	Fastqsanger.gz
	SRR6714660_2.fastq.gz	Fastqsanger.gz
	SRR6714661_1.fastq.gz	Fastqsanger.gz
	SRR6714661_2.fastq.gz	Fastqsanger.gz
	SRR6714662_1.fastq.gz	Fastqsanger.gz

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miR-24 induces human T cell exhaustion though mitochondria energy metabolic reprograming via suppressing MYC and FGF11

Project description:Exhausted T cells (TExh) is a barrier for cancer immunotherapy, evidences demonstrate that transcriptional regulation is essential for TEX induction; however the factors that manipulate exhausted phenotype are largely unexplored. Here we showed that the microRNA (miR)-24, previously established to be enriched in eoxosmes from nasopharyngeal carcinoma (NPC) cells and promote T cell dysfunction, induced T cells to express high level of TIM-3, PD-1 and CD39 but to display low IFNg and GrB secretion and diminished proliferation ability ( a TExh phenotype) through inhibiting energy metabolism in vitro. Forced miR-24 expression inhibited ATP production through mitochondrial oxidative phosphorylation, while blockade of endogenous miR-24 the mitochondrial formation became massive and tubular and the levels of mitochondrial constituent proteins including Mfn1, Mfn2, P-Drp1 and TOMM20 was increased in OKT-3 stimulated T cells. MiR-24-mediated TEX and mitochondria metabolism reprogramming were regulated by suppressing MYC and FGF11 expression. Moreover, MYC enhanced the FGF11 transcription to promote mitochondria ATP production. Importantly, clinical data showed an increased TEX phenotype in circuiting and tumor-infiltrating T cells from NPC patients. Thus, our findings support that inhibition of miR-24-mediated mitochondria metabolism reprogramming can be titrated to break TExh immune barrier in NPC immunotherapy.

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Project description:Crosstalk from Non-Cancerous Mitochondria Can Inbibit Tumor Properties of Metastatic Cells by Suppressing Oncogenic Pathways

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Disturbed mitochondrial dynamics in CD8+ TIL reinforce epigenetic programming linked with T cell exhaustion

Project description:The metabolic challenges present in tumors attenuate the metabolic fitness and anti-tumor activity of tumor-infiltrating T lymphocytes (TILs). However, it remains unclear whether persistent metabolic insufficiency can imprint permanent T cell dysfunction. We found that TILs accumulating depolarized mitochondria as a result of declined mitophagy activity display functional, transcriptomic and epigenetic characteristics of terminally exhausted T cells. Mechanistically, declined mitochondrial fitness in TILs is induced by the coordination of T cell receptor stimulation, microenvironmental stressors and PD-1 signal. Forcing the accumulation of depolarized mitochondria with pharmacological interventions induces epigenetic reprogramming for terminal exhaustion, indicating that mitochondrial deregulation is indeed a cause – rather than a consequence – of T cell exhaustion. Furthermore, supplementation with nicotinamide riboside enhances T cell mitochondrial fitness and improved responsiveness to anti-PD-1 treatment. Together, our results reveal new insights on how mitochondrial dynamics and quality orchestrate T cell anti-tumor responses and commitment to the exhaustion program.

2020-09-01 | GSE144583 | GEO

Disturbed mitochondrial dynamics in CD8+ TIL reinforce epigenetic programming linked with T cell exhaustion

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GDNPs reprogram macrophages to regulate arginase-1 release for ameliorating T cell exhaustion in tumor microenvironment

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