@techreport{oai:mie-u.repo.nii.ac.jp:00011743,
 author = {石井, 健一朗 and Ishii, Kenichiro and 白石, 泰三 and Shiraishi, Taizo and 広川, 佳史 and Hirokawa, Yoshifumi and 杉村, 芳樹 and Sugimura, Yoshiki},
 month = {May},
 note = {application/pdf, CAFsは増殖因子やサイトカインの産生などを介し、癌の進展を様々な側面から促進させる。そのため、我々は癌細胞の増殖抑制に加えて、CAFsの働きを阻止することができれば、より効率的に癌の進展を抑制することが可能になると考えている。本検討により、CAFsは癌細胞と同様に正常な線維芽細胞を活性化し、CAF様の性状を誘導することが明らかとなった。さらにCAFsによるパラクライン作用は極めて不均一であることが明らかとなり、これは前立腺癌間質が不均一であることを意味する、すなわち臨床的にも前立腺の組織構造を考慮した前立腺癌治療の必要性を強く示唆するものであった。, Carcinoma-associated fibroblasts (CAFs) are activated fibroblasts that support the proliferation and invasion of adjacent cancer cells. In the tumor microenvironment, CAFs communicate not only with cancer cells but also surrounding stromal cells. In this study, we performed in vitro co-culture experiments using commercially available normal human prostate stromal cells PrSC and primary cultures of human prostate fibroblasts (pcPrFs) derived from prostate cancer patients. In PrSC, protein productions of TGFb1, IL-6, and VEGF were significantly increased by co-culturing with pcPrFs. Similarly, those of IL-6 and VEGF in pcPrFs were significantly increased by co-culturing with PrSC. In PrSC, mRNA expressions of growth factor were significantly increased by co-culturing with pcPrFs. Those of growth factor in pcPrFs were significantly increased by co-culturing with PrSC. Here our results demonstrated that interactions between PrSC and pcPrFs showed quite heterogeneous., 2013年度～2015年度科学研究費補助金(基盤研究(C))研究成果報告書, 25462475},
 title = {細胞競合により制御される前立腺癌間質リモデリングの解明},
 year = {2016},
 yomi = {イシイ, ケンイチロウ and シライシ, タイゾウ and ヒロカワ, ヨシフミ and スギムラ, ヨシキ}
}