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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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Project description:Lenvatinib targets multiple oncogenic kinases including vascular endothelial growth factor receptors (VEGFRs) and showed longer median progression-free survival than sorafenib, the only approved treatment for >10 years. With the successful combination therapy of anti-PD-L1 pembrolizumab and anti-VEGF bevacizumab for advanced HCC as well as encouraging experimental findings, lenvatinib was also expected to enhance anti-tumor effects by combining anti-PD-1 pembrolizumab compared to lenvatinib alone; however, the phase III clinical trial failed to show their synergetic survival benefits, highlighting the need for elucidating its mode of action in human HCC specimens after lenvatinib treatment. We performed multi-layer transcriptome analyses of surgically resected human HCC samples after lenvatinib treatment as a neo-adjuvant therapy using RNA-sequencing. Molecular pathway analyses and immunohistochemistry revealed that VEGF-mediated aberrant vascularity and cytotoxic GZMK+CD8 T cells infiltration were significantly improved in lenvatinib-treated HCC; however, the majority of these cytotoxic T cells were trapped in the intratumor fibrotic stroma, suggesting that lenvatinib-treated HCC is in the so-called excluded condition. Excluded tumors are generally believed to be less responsive to immune checkpoint inhibitors, which might be the reason the combination therapy failed to show the additive benefits.

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