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

研究成果: ジャーナルへの寄稿学術論文査読

17 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)4359-4370
ページ数12
ジャーナルCancer science
111
12
DOI
出版ステータス出版済み - 12-2020

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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