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Exhausted CD8+ T cells overexpress CCL5 during combination therapy to mediate resistance of hepatoma cells to lenvatinib: one situation may contribute to the survival of residual tumor cells

ABSTRACT: Exhausted CD8+ T cells overexpress CCL5 during combination therapy to mediate resistance of hepatoma cells to lenvatinib: one situation may contribute to the survival of residual tumor cells

PROVIDER: PRJNA1032628 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26538800_1.fastq.gz	Fastqsanger.gz
	SRR26538800_2.fastq.gz	Fastqsanger.gz
	SRR26538801_1.fastq.gz	Fastqsanger.gz
	SRR26538801_2.fastq.gz	Fastqsanger.gz
	SRR26538802_1.fastq.gz	Fastqsanger.gz

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Exhausted CD8+ T cells overexpress CCL5 during combination therapy to mediate resistance of hepatoma cells to lenvatinib: one situation may contribute to the survival of residual tumor cells

Project description:In conclusion, we discovered that during combination therapy, tumor tissue demonstrated a more active metabolic reprogramming than normal liver tissue, as indicated by a significant upregulation of CYP1A1 expression. In addition, we validated that CD8T cells secreted more CCL5 after treatment, which upregulated CYP1A1 expression by binding to CCR5, leading to resistance of hepatoma cells to lenvatinib. Finally, we demonstrated that interference with the CCL5/CCR5/CYP1A1 pathway can enhance the efficacy of lenvatinib and combination therapy.

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