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Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

ABSTRACT: Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

PROVIDER: PRJNA1190985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31518900_1.fastq.gz	Fastqsanger.gz
	SRR31518900_2.fastq.gz	Fastqsanger.gz
	SRR31518901_1.fastq.gz	Fastqsanger.gz
	SRR31518901_2.fastq.gz	Fastqsanger.gz
	SRR31518902_1.fastq.gz	Fastqsanger.gz

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Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

Project description:Despite significant advancements in cancer immunotherapy, many patients continue to respond poorly. Novel therapeutic strategies and drugs are urgently needed. Here, we found that CYP2E1 is significantly upregulated in M2 macrophages. The CYP2E1 inhibitor, Q11, could inhibit M2 macrophage polarization, while CYP2E1 overexpression could promote it. Increased levels of CYP2E1 and M2 macrophages in the tumor microenvironment of HCC patients correlate with poor prognosis. Q11 could inhibit tumor cells by targeting M2 macrophages rather than directly attacking tumor cells. Both Q11 and Cyp2e1 knockout could effectively suppress tumor growth. Q11 reduces the production of CYP2E1 metabolites (±)9(10)-DiHOME and (±)12(13)-DiHOME, thus attenuating PPARγ activation and M2 macrophage polarization. In summary, our findings suggest that Q11 could suppress M2 macrophage polarization by modulating the CYP2E1/(±)9(10)-DiHOME or (±)12(13)-DiHOME/PPARγ axis, indicating that CYP2E1 inhibition may be a novel therapeutic strategy for HCC and positioning Q11 as a promising therapeutic agent.

2024-12-26 | GSE282907 | GEO

Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization.

Project description:Despite significant advancements in cancer immunotherapy, many patients continue to respond poorly. Novel therapeutic strategies and drugs are urgently needed. Here, we found that CYP2E1 is upregulated in M2 macrophages. The CYP2E1 inhibitor, Q11, could inhibit M2 macrophage polarization, while CYP2E1 overexpression could promote it. Increased levels of CYP2E1 and M2 macrophages in the tumor microenvironment of HCC patients correlate with poor prognosis. Q11 could inhibit tumor cells by targeting M2 macrophages rather than directly attacking tumor cells. Both Q11 and Cyp2e1 knockout could effectively suppress tumor growth. Q11 reduces the production of CYP2E1 metabolites ( ±)9(10)-DiHOME and ( ±)12(13)-DiHOME, thus attenuating PPARγ activation and M2 macrophage polarization. In summary, our findings suggest that Q11 could suppress M2 macrophage polarization by modulating the CYP2E1/( ±)9(10)-DiHOME or ( ±)12(13)-DiHOME/PPARγ axis, indicating that CYP2E1 may be a potential therapeutic target for HCC, and its inhibitor Q11 may be a potential drug for the treatment of HCC.

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Total RNA-seq using mouse tissues from Cyp2e1 +/+ mice upon pair-fed, Cyp2e1 +/+ mice upon EtOH-fed, Cyp2e1 -/- mice upon pair-fed, and Cyp2e1 -/- mice upon EtOH fed.

Project description:To investigate the effect of Cyp2e1 and EtOH on mRNA expression in mouse tissues, we profiled total RNA expression using mouse tissues from Cyp2e1 -/- mice and Cyp2e1 +/+ mice upon EtOH fed mice compared to control. We compare the expression level of RNA and profile circular RNA expression using circular RNA junction.

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Pseudomonas sp. Q11

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Total RNA-seq using mouse tissues from Cyp2e1 +/+ mice upon pair-fed, Cyp2e1 +/+ mice upon EtOH-fed, Cyp2e1 -/- mice upon pair-fed, and Cyp2e1 -/- mice upon EtOH fed.

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Activation and presentation of SIINFEKL:Kb by lung CD11b+ and CD103+ DCs after intranasal SIIN-Q11.

Project description:To investigate whether differentially expressed genes induced by SIIN-Q11 were shared between lung CD11b+ and CD103+ DCs, we performed gene expression profiling analysis of lung CD11b+ and CD103+ DCs after intranasal SIIN-Q11.

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