【Major Papers of the Laboratory】
・Roles of bone morphogenetic protein type I receptors and Smad proteins in osteoblast and chondroblast differentiation., Mol Biol Cell, 10, 3801, 1999
・SNIP1 is a candidate modifier of the transcriptional activity of c-Myc on E box-dependent target genes., Molecular cell, 24(5), 2006
・TGF-beta synergizes with defects in the Hippo pathway to stimulate human malignant mesothelioma growth, The Journal of experimental medicine, 209(3), 2012
・BMP and activin membrane-bound inhibitor regulate connective tissue growth factor controlling mesothelioma cell proliferation, BMC Cancer, 22(1), 2022
・Activation of platelet-derived growth factor receptors regulate connective tissue growth factor protein levels via the AKT pathway in malignant mesothelioma cells, J Biochem, 176(6), 2024

【Education】
We are in charge of the following lectures for students in the Department of Dentistry: Cell Science (Liberal Arts Education Program), Genomic Medicine (Program of Dentistry), Cancer Cell Biology (Program of Dentistry; starting from 2021), Development of International Collaboration in Medical Science (Liberal Arts Education Program), International Future Dentistry with the Outcomes of Researches (Program of Dentistry), Introductory Japanese Culture (Program of Dentistry; for international students), Overview of Dentistry (Program of Dentistry; for international students), Life Science (Program of Dentistry; for international students)

【Research】
Our laboratory is dedicated to elucidating the molecular mechanisms underlying refractory tumors such as malignant mesothelioma and mucosal melanoma, and to identifying novel therapeutic targets. In malignant mesothelioma, abnormalities in the NF2 (neurofibromatosis type 2) gene and its downstream Hippo signaling pathway are known to enhance the expression of CTGF (Connective Tissue Growth Factor) in cooperation with TGF-β (Transforming Growth Factor-β), thereby promoting tumor growth. 
Moreover, we have discovered a novel regulatory mechanism in which the PDGFR–AKT signaling axis increases CTGF protein levels through translational control, independent of changes in mRNA abundance. We are currently working toward the development of therapeutic strategies targeting both the TGF-β–CTGF and PDGFR–AKT–CTGF pathways. 
We are also engaged in bioinformatics analyses using RNA-seq and genomic data to identify biomarkers associated with tumor aggressiveness and patient prognosis, as well as to explore potential therapeutic targets. 
By integrating cellular and molecular biology approaches with computational science, and through active interdisciplinary collaborations, we aim to contribute to the development of innovative treatment strategies for refractory cancers.