Single-cell data derived from metastatic murine liver tissues from the B16-spleen-liver melanoma liver metastasis model (three biological replicates (n1, n2, n3)).

Approved RNAi therapeutics marked groundbreaking advances. Yet, the clinical translation of RNAi for cancer treatment remains unrealized - largely due to the predominant delivery of siRNAs to hepatocytes. Our study uncovers a previously unrecognized crosstalk mechanism that shapes the metastatic liver niche, offering a compelling opportunity to transform this apparent limitation into a therapeutic advantage. By selectively targeting NPY expression in hepatocytes, rather than in tumor cells, we introduce a novel paradigm for the treatment of hepatic metastases. The here uploaded data are derived from single-nucleus RNA-seq (three biological replicates (n1, n2, n3) of the metastatic microenvironment applying the B16-melanoma cell spleen-liver metastasis mouse model.