Galectin-1 (Gal1), a glycan-binding protein, plays a key role in the creation of an immunosuppressed tumour microenvironment (TME) acting as a negative regulator of the immune response, fostering tumour immune escape, and stimulating an invasive, stem-like phenotype, enhancing dissemination in cancer. Our group focuses on the TME in breast cancer, which has the highest incidence amongst women worldwide. To further study the role of Gal1 in mammary tumour progression and metastasis, we developed a transgenic model using MMTV-PyMT mice WT or KO for lgals1-/- (PYMT-KO). Using this experimental model, we observed that PyMT-KO mice present an increased latency in tumour burden and a longer tumour-free survival time, with a lower number of transformed ducts and lung metastasis, alongside a reduced mammary gland branching morphogenesis (whole mount). 
In hopes of understanding the role that Gal1 plays in mammary glands, we performed cell sorting based on surface markers EPCAM and CD49f to categorize the isolated mammary cells from WT and KO mice into four main populations: luminal, basal, stromal, and mammary stem cells (MaSC). We observed that lgals1-/- KO mice present a decreased percentage of luminal and MaSC cells in comparison to the Gal1 sufficient strain, which presents an enriched population of basal cells (spectral FACS). Each population’s purity was evaluated by Real Time PCR using specific markers and we notoriously point out a reduction in the expression of progesterone receptor in the mammary gland and in the luminal population in the lgals1-/- KO mice. By scRNAseq (in silico analysis) and qPCR, we found that Gal1 is synthesized by basal cell lineages and MaSC cells, which may in turn promote branching morphogenesis. Our findings highlight the relevance of Gal1 in regulating normal mammary gland morphogenesis and assert its critical role in metastatic spreading in breast cancer.