Extended Data Fig. 4: Additional description of residual AKTP and AKP metastatic cells.
From: Metastatic recurrence in colorectal cancer arises from residual EMP1+ cells
a, UMAPs of colorectal primary tumours and liver metastases at different stages (micro, small and large) coloured according to sequencing batch, mouse ID, and sample ID. b, UMAPs showing the expression levels of coreHRC, EpiHR, and mKi67 gene signatures and Lgr5 and Krt20 genes. c, Violin plots showing expression of relevant genes used to define the 6 different Seurat clusters. d, Fraction of cells (y axis) from each Seurat cluster (x axis) present in the different sample types: Primary Tumour, micro-, small- and macro- metastases according to the indicated color code. Note the “HRCs Krt20-” are mostly exclusive from micro metastases samples, whereas Lgr5+ cells are highly enriched in small metastases samples. e, Smoothed Krt20 gene and partial EMT gene signature17 expression trends fitted with Generalized Additive Models as a function of pseudotime in primary tumours, micro+small and large metastases. f, g, UMAP of AKP liver micrometastases coloured according to timing of profiling and Seurat clusters. h, Barplot showing proportion of different Seurat tumour cell types captured in AKP early vs late micrometastases. i-l, UMAPs showing the expression levels of the coreHRC, mKi67 and Mex3a gene signatures and Lgr5 mRNA in AKP metastases. m, Barplot showing Seurat cluster distribution across AKP early and late micrometastases. n. Violin plots showing expression levels of the Mex3a signature16 in AKP early and late micrometastases versus AKTP micro and small metastases. o, Vector fields representing RNA velocity projected on UMAPs of AKP micrometastases, coloured by the pseudotime estimated for each cell with scVelo. p, Smoothed coreHRC, mKi67, and Lgr5 gene signature expression trends in the early and late AKP micrometastasis dataset fitted with generalized additive models as a function of CellRank pseudotime.
