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In vivo study of the Tim3-loss in breast cancer cells during metastasis

ABSTRACT: In metastasis, the existence tumor cells overcoming the immune system during early organ seeding is crucial, yet the dynamics of tumor-immune interactions during micrometastasis remain unclear. Examining the immune selective pressure in breast cancer (BC) mouse models, we unexpectedly found TIM3 among the most upregulated genes in metastatic surviving BC cells. The selection of TIM3+ tumor cells, was specifically occurring during early seeding of micrometastasis, escaping the immune attack and acquiring stemness. Also clinical data confirmed increased TIM3+ tumor cells in BC metastasis. The aim of the study was to understand the mechanistic insgihts of Tim3 in breast cancer cells in vivo to decipher pivotal pathways of Tim3-mediated immun-evasion.

ORGANISM(S): Mus musculus

PROVIDER: GSE260480 | GEO | 2025/07/02

REPOSITORIES: GEO

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Project description:We established a model of human melanoma metastasis to identify differentially expressed genes in brain metastasis, compared to cutaneous melanoma from which they were developed. Such genes may control brain metastasis. The identification and characterization of these genes would advance the understanding of the metastatic process and may lead to new diagnostics and therapeutic approach. Brain metastases occur in almost 40% of melanoma patients. The median survival of such patients does not exceed a few months. Very little information is available on mechanisms underlying the progression of melanoma towards brain metastasis. The function, and significance of the various factors involved in melanoma progression must be deciphered using relevant models. Currently, most human melanoma brain metastasis models consist of xenografted cells inoculated into immune-deficient mice mainly by intracarotid or intra-cardiac administration. We generated a reproducible melanoma brain metastasis model, consisting of brain-metastasizing variants and local, sub-dermal variants that originate from the same melanomas thus sharing a common genetic background. The brain metastasizing variants were obtained by intra-cardiac inoculation. One of the brain metastasizing variants when inoculated sub-dermally yielded spontaneous brain dormant micrometastasis. Cells from the spontaneous brain micrometastasis when removed from the brain microenvironment proliferate very well in vitro and generate tumors in the skin being the orthotopic organ site. The brain metastasis and micro-metastasis cells expressed higher levels of ANGPTL4, COX-2, MMP1, MMP2 and PRAME and lower levels of CLDN1, CYR61 and IL-6R than the cutaneous variants. These gene products may be involved in melanoma brain metastasis and may serve as novel brain metastasis biomarkers and targets for therapy. 8 Samples (arrays) were analyzed. We generated pairwise comparisons between cutaneous and brain metastatic variants of the same genetic background, using Partek Genomics Suite, in the three melanoma models. Genes with pM-bM-^IM-$5% and a fold-change difference of M-bM-^IM-%1.25 or <-1.25 were selected.

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In vivo study of the Tim3-loss in breast cancer cells during metastasis

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