Upregulation of S100A10 in metastasized breast cancer stem cells

Hisano Yanagi, Takashi Watanabe, Tatsunori Nishimura, Takanori Hayashi, Seishi Kono, Hitomi Tsuchida, Munetsugu Hirata, Yuko Kijima, Shintaro Takao, Seiji Okada, Motoshi Suzuki, Kazuyoshi Imaizumi, Kenji Kawada, Hironobu Minami, Noriko Gotoh, Yohei Shimono

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


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, S100A10 regulated the matrix metalloproteinase activity and the expression levels of stem cell–related genes. Finally, constitutive knockdown of S100A10 significantly reduced their metastatic ability to the liver in vivo. These findings suggest that S100A10 functions as a metastasis promoter of breast CSCs by conferring both invasion ability and CSC properties in breast cancers.

Original languageEnglish
Pages (from-to)4359-4370
Number of pages12
JournalCancer science
Issue number12
Publication statusPublished - 12-2020

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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