Yosuke Mitsui^*†, Nahoko Tomonobu^*, Masami Watanabe^†, Rie Kinoshita^*, I Wayan Sumardika^*‡, Chen Youyi^*, Hitoshi Murata^*, Ken-ichi Yamamoto^*, Takuya Sadahira^†, Acosta Gonzalez Herik Rodrigo^*†, Hitoshi Takamatsu^*, Kota Araki^*§, Akira Yamauchi^¶, Masahiro Yamamura^#, Hideyo Fujiwara^**, Yusuke Inoue^††, Junichiro Futami^‡‡, Ken Saito^§§, Hidekazu Iioka^§§, Eisaku Kondo^§§, Masahiro Nishibori^¶¶, Shinichi Toyooka^§, Yasuhiko Yamamoto^##, Yasutomo Nasu^†, Masakiyo Sakaguchi^*

Oncology Research, Vol.27, No.8, pp. 945-956, 2019, DOI:10.3727/096504019X15555408784978

Abstract S100A11, a member of the S100 family of proteins, is actively secreted from pancreatic ductal adenocarcinoma (PDAC) cells. However, the role of the extracellular S100A11 in PDAC progression remains unclear. In the present study, we investigated the extracellular role of S100A11 in crosstalking between PDAC cells and surrounding fibroblasts in PDAC progression. An abundant S100A11 secreted from pancreatic cancer cells stimulated neighboring fibroblasts through receptor for advanced glycation end products (RAGE) upon S100A11 binding and was followed by not only an enhanced cancer cell motility in vitro but also an increased number of the PDAC-derived circulating tumor cells (CTCs) in… More >

Hitoshi Takamatsu^*1, Ken-ichi Yamamoto^*1, Nahoko Tomonobu^*, Hitoshi Murata^*, Yusuke Inoue^†, Akira Yamauchi^‡, I Wayan Sumardika^*§, Youyi Chen^*, Rie Kinoshita^*, Masahiro Yamamura^¶, Hideyo Fujiwara^#, Yosuke Mitsui^{*, **}, Kota Araki^*††, Junichiro Futami^‡‡, Ken Saito^§§, Hidekazu Iioka^§§, I Made Winarsa Ruma^§, Endy Widya Putranto^¶¶, Masahiro Nishibori^##, Eisaku Kondo^§§, Yasuhiko Yamamoto^***, Shinichi Toyooka^††, Masakiyo Sakaguchi^*

Oncology Research, Vol.27, No.6, pp. 713-727, 2019, DOI:10.3727/096504018X15433161908259

Abstract The fertile stroma in pancreatic ductal adenocarcinomas (PDACs) has been suspected to greatly contribute to PDAC progression. Since the main cell constituents of the stroma are fibroblasts, there is crosstalking(s) between PDAC cells and surrounding fibroblasts in the stroma, which induces a fibroblast proliferation burst. We have reported that several malignant cancer cells including PDAC cells secrete a pronounced level of S100A11, which in turn stimulates proliferation of cancer cells via the receptor for advanced glycation end products (RAGE) in an autocrine manner. Owing to the RAGE⁺ expression in fibroblasts, the extracellular abundant S100A11 will affect adjacent fibroblasts. In this… More >