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Effect of anti-tumor efficacy of depletion of Nrf2 in effector T cells

ABSTRACT: Effect of anti-tumor efficacy of depletion of Nrf2 in effector T cells

PROVIDER: PRJNA956941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24206418_1.fastq.gz	Fastqsanger.gz
	SRR24206418_2.fastq.gz	Fastqsanger.gz
	SRR24206419_1.fastq.gz	Fastqsanger.gz
	SRR24206419_2.fastq.gz	Fastqsanger.gz
	SRR24206420_1.fastq.gz	Fastqsanger.gz

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Effect of anti-tumor efficacy of depletion of Nrf2 in effector T cells

Project description:To investigate the function of Nrf2-deficient CD8 T cells in the regulation of anti-tumor response, we established adoptive transfer models. We then performed gene expression profiling analysis using data obtained from RNA-seq of Nrf2-deficient and WT CD8 T cells in the tumor.

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Project description:Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy; however, their use is frequently associated with immune-related adverse events (irAEs). In this study, anti-PD-L1 therapy exacerbates muscle wasting in tumor-bearing male mice despite its anti-tumor efficacy, accompanied by an accumulation of CD8+ T cells in muscle. Single-cell RNA sequencing identifies these cells as tissue-resident memory-like CD49a+ CD8+ T cells. While CD8+ T cell depletion prevents muscle wasting, it compromises the anti-tumor efficacy of anti-PD-L1. To resolve this paradox, we identify cathepsin L (CTSL) as a dual-target capable of suppressing both tumor progression and CD8+ T cell-mediated muscle wasting, through integrative transcriptomic analysis. Pharmacological inhibition of CTSL not only mitigates anti-PD-L1-induced muscle wasting but also further suppresses tumor growth, potentially via downregulation of BNIP3. Here, we show that CTSL is a dual-action target to uncouple anti-tumor efficacy from muscle-specific irAEs, offering a strategy to improve clinical outcomes of ICIs.

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Aberrant Nrf2 activation delays erythroid maturation during chemotherapeutic drug-induced erythropoiesis

Project description:Nuclear factor (erythroid-derived 2)-like2 (Nrf2) and miR-144/451 regulate two well-established systems that have been identified to maintain redox homeostasis in erythroid cells by removing excess reactive oxygen species (ROS). Whether Nrf2 plays a role in the differentiation process during erythropoiesis has not been reported. In this study, we demonstrate that miR-144/451 gene knockout (KO) in mice dampens erythroid differentiation when 5-Fluorouridine is used to induce acute anemia. Surprisingly, inactivation of Nrf2 by crossing Nrf2 KO mice completely alleviates the delayed erythropoiesis in miR-144/451 KO mice. Nrf2 is a miR-144/451 target and depletion of miR-144/451 leads to the derepression of Nrf2, and thus an overexpression of Nrf2. Therefore, our findings indicate that persistent Nrf2 activation blocks erythroid maturation. We further reveal that even physiological levels of Nrf2 impair the erythroid differentiation. The underlying mechanism is that hyperactivity of Nrf2 leads to the sustained proliferation of erythroblasts partially by activation of Myc signaling. We also find that Nrf2 and miR-144/451 coordinate to scavenge ROS but do not phenotypically copy each other, indicating that they control two distinct anti-oxidant systems in erythroid cells. Furthermore, we find that miR-144/451 deficiency produces a more profound defect of erythropoiesis than dysfunctional Nrf2. Given that Nrf2 is ubiquitously expressed in tumor tissues, which facilitates cancer malignancy and chemoresistance; and that cancer is often accompanied by anemia that markedly inhibits antineoplastic treatment efficacy and anticancer immunity, our findings suggest that targeting Nrf2 holds great promise that not only harms cancer cells, but also reverses cancer-related anemia.

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