Therapeutic Perspective of Tumor Microenvironment in Non-Small Cell Lung Cancer

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592090
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Thoracic surgery
• Research Institution: Osaka University
• Principal Investigator: SHINTANI yasushi 大阪大学, 医学(系)研究科(研究院), 講師 (90572983)
• Co-Investigator(Kenkyū-buntansha): OKUMURA Meinoshin 大阪大学, 医学系研究科, 教授 (40252647) ; MINAMI Masato 大阪大学, 医学部附属病院, 准教授 (10240847) ; SAWABATA Noriyoshi 大阪大学, 医学系研究科, 准教授 (50403184) ; INOUE Masayoshi 大阪大学, 医学系研究科, 准教授 (10379232) ; NAKAGIRI Tomoyuki 大阪大学, 医学系研究科, 招へい教員 (70528710) ; KAWAMURA Tomohiro 大阪大学, 医学系研究科, 助教 (30528675)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 肺癌 / 癌周囲微小環境 / 癌幹細胞 / 治療抵抗性 / 上皮間葉移行

Outline of Final Research Achievements

Our recent focus has been signaling pathways that promote Epithelial to mesenchymal transition (EMT) in response to tumor microenvironment such as growth factors as well as extracellular matrix. Tumor stroma in non-small cell lung cancer (NSCLC) is of interest in the entity as both biomarkers and therapy targets. We can assume that anticancer therapeutics targeting EMT pathways and signaling elements will bring additional ways for the treatment of NSCLC. IL-6 from tumor stroma enhanced epithelial cell EMT and acquisition of cancer stemness by enhancing TGF-beta signaling. IL-6 and TGF-beta may play contributing roles in maintenance of the paracrine loop between these two cytokines as part of the communication between tumor stroma and NSCLC cells, resulting in chemoresistance.

Free Research Field

肺癌