Novel therapeutic strategy for sarcomas by targeting PPRX1 positive cancer stem-like cells

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K18449
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor therapeutics
• Research Institution: Okayama University (2017); Nigata University of Phermacy and Applied Life Sciences (2015-2016)
• Principal Investigator: Yamada Daisuke 岡山大学, 医歯薬学総合研究科, 助教 (50733680)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: セマフォリン / 肺がん / がん幹細胞 / mTORシグナル / 薬剤耐性 / EGFR阻害剤

Outline of Final Research Achievements

In this study, we studied the oncogenic role of semaphorin 3A to establish the novel therapeutic strategy against lung cancer. Inhibition of semaphorin 3A signaling by shRNA system in lung cancer cells decreased their proliferative capacity and increased the sensitivity to EGFR inhibitors. Furthermore, the self-renewal or tumorigenic capacity of cancer stem-like cells, the origin of cancer, was completely abolished by the inhibition of semaphorin 3A signaling. These results demonstrate that the inhibition of semaphorin 3A signaling not only releases the resistance to several drugs but also eradicates cancer stem-like cell in lung cancer.

Free Research Field

腫瘍生物学