Roles of MafK-Gpnmb axis in malignant progression of cancer and molecular targeted therapy

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19070
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Experimental pathology
• Research Institution: University of Tsukuba
• Principal Investigator: OKITA Yukari 筑波大学, 医学医療系, 研究員 (30743710)
• Research Collaborator: KATO Mitsuyasu 筑波大学, 医学医療系, 教授 (20194855)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: MafK / GPNMB / 腫瘍形成 / EMT / 転移形成 / 分子標的治療

Outline of Final Research Achievements

Previously we showed that the transcription factor MafK is involved in induction of epithelial-mesenchymal transition (EMT) and malignant progression of breast cancer cells. Furthermore, we identified glycoprotein nmb (GPNMB) as a target of MafK, which also has the functions as an inducer of EMT and tumorigenesis.
In this project, we further investigated the molecular mechanisms how MafK-GPNMB axis contributes to EMT induction and tumorigenesis. Then, we found post-translational modification of MafK is important for functional regulation of MafK in EMT induction and tumorigenesis. Moreover, we identified some domains or motifs which are essential for GPNMB-mediated EMT induction and tumorigenesis. We are going to investigate further detail mechanisms in order to find new target for breast cancer treatment.

Free Research Field

腫瘍学