biostudies-literatureYanagi HJapan Society for the Promotion of Science LondonCancer Research Institute of Kanazawa UniversityPrincess Takamatsu Cancer Research FundFujita Health UniversityPromotion and Mutual Aid Corporation for Private Schools of JapanJapan Society for the Promotion of Science4359-4370https://www.ebi.ac.uk/biostudies/studies/S-EPMC7734155biostudies-literatureUnknown111(12)Metastatic progression remains the major cause of death in human breast cancer. Cancer cells with cancer stem cell (CSC) properties drive initiation and growth of metastases at distant sites. We have previously established the breast cancer patient-derived tumor xenograft (PDX) mouse model in which CSC marker CD44⁺ cancer cells formed spontaneous microscopic metastases in the liver. In this PDX mouse, the expression levels of S100A10 and its family proteins were much higher in the CD44⁺ cancer cells metastasized to the liver than those at the primary site. Knockdown of S100A10 in breast cancer cells suppressed and overexpression of S100A10 in breast cancer PDX cells enhanced their invasion abilities and 3D organoid formation capacities in vitro. Mechanistically, S100ACancer scienceUpregulation of S100A10 in metastasized breast cancer stem cells.PMC773415515K1438118K07231 : 19K23900: 20K07600Watanabe TKawada KYanagi HTsuchida HSuzuki MKijima YGotoh NHayashi TImaizumi KHirata MKono SMinami HShimono YTakao SOkada SNishimura TfalseUpregulation of S100A10 in metastasized breast cancer stem cells.Metastatic progression remains the major cause of death in human breast cancer. Cancer cells with cancer stem cell (CSC) properties drive initiation and growth of metastases at distant sites. We have previously established the breast cancer patient-derived tumor xenograft (PDX) mouse model in which CSC marker CD44⁺ cancer cells formed spontaneous microscopic metastases in the liver. In this PDX mouse, the expression levels of S100A10 and its family proteins were much higher in the CD44⁺ cancer cells metastasized to the liver than those at the primary site. Knockdown of S100A10 in breast cancer cells suppressed and overexpression of S100A10 in breast cancer PDX cells enhanced their invasion abilities and 3D organoid formation capacities in vitro. Mechanistically, S100A2020-01-01T00:00:00Z2020 Dec2026-05-03T08:22:03.12Z2021-02-20T14:28:51ZS-EPMC77341553297666110.1111/cas.14659