Elucidation of the mechanisms of carcinogenesis regulated by oxidative stress response

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08438
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Chiba Cancer Center (Research Institute)
• Principal Investigator: WAKABAYASHI Yuichi 千葉県がんセンター(研究所), 発がん研究グループ 実験動物研究室, 室長 (40303119)
• Co-Investigator(Kenkyū-buntansha): 磯貝 恵理子 千葉県がんセンター(研究所), 発がん研究グループ 実験動物研究室, 上席研究員 (40300917)
• Co-Investigator(Renkei-kenkyūsha): SAKAKIBARA Yasubumi 慶応義塾大学, 理工学部, 教授 (10287427)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: Meis1 / Stk25 / 皮膚発がん

Outline of Final Research Achievements

Meis1 has been shown to play an important role in leukemogenesis. However, its functions in skin carcinogenesis remain poorly understood. The c-Met inhibitor SU11274 has been identified through drug screening with HOXA9/Meis1-induced AML cell lines. We treated Meis1 knockdown cells with SU11274. As a result, SU11274 suppressed cell proliferation only in the presence of Meis1. In addition, to investigate the downstream genes of Meis1, we carried out ChIP sequencing analysis using chemically induced skin tumors. We carried out the luciferase assay with the promoter region of Stk25, one of Meis1 downstream candidate genes. As a result, strong luciferase activity was detected when B9 cells were transfected with the luciferase construct and full length Meis1 vector. We then generated Stk25 knockdown cell lines and did the invasion assay. As a result, Stk25 knockdown cells showed the reduction of the invasion activity as Meis1 knock down cell lines did.

Free Research Field

マウス遺伝学