The effect of BACH1 on malignant transformation of tumor

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K07108
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Tohoku University
• Principal Investigator: Matsumoto Mitsuyo 東北大学, 医学系研究科, 助教 (80400448)
• Research Collaborator: SATO masaki ; IGARASHI kazuhiko
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: BACH1

Outline of Final Research Achievements

BTB and CNC homolog 1 (BACH1) promotes transformation, cell proliferation and tumor formation in a model of activated RAS transfected-mouse embryonic fibroblasts (MEFs). We focused on the role of BACH1 in the pancreatic ductal adenocarcinoma (PDAC) more than 90% of which has KRAS mutation. Although BACH1 did not affect cell proliferation and tumor growth, but promoted migration ability and invasion ability in vitro and metastasis in vivo. We revealed that BACH1 repressed directly the expression of multiple epithelial-related genes as its mechanism. We showed also BACH1 is a poor prognostic factor on PDAC.

Free Research Field

分子腫瘍学

Academic Significance and Societal Importance of the Research Achievements

膵癌は最も予後不良な悪性腫瘍の１つである。その原因の１つである腫瘍の悪性形質転換の機序については未だ未解明な点も多い。本研究から腫瘍の悪性形質転換のステップと考えられている上皮間葉転換を、BACH1が直接複数の上皮系遺伝子の転写を抑制することで促すことが示唆された。実際にBACH1高発現膵癌患者の予後は不良であり、BACH1が膵癌の治療標的となり得る可能性を示した点で、その意義は高いと考える。