Makoto Noda, Ph.D. Professor
Tumors arise in a wide variety of animals, from insects to men, and yet some animals (such as C. elegans and flat warm) are free from tumors. Why tumor cells rely on the pathway (glycolysis) inefficient in extracting energy from nutrients remains a mystery for more than a half century. Solving such interesting puzzles may lead to the discovery of innovative approaches in cancer eradication. Armed with modern technologies, such as mouse genetics, omics analyses, and bio-molecular imaging, we try to understand the molecular mechanisms of carcinogenesis and tumor suppression.
Research and Education
In searching for the molecules suppressing malignant phenotypes of cancer cells, we discovered a regulator of extracellular matrix-remodeling named RECK. RECK is downregulated in various common cancers, while it is required for mammalian embryogenesis. Our current projects includes (1) mechanism of RECK’s actions in tumor suppression, (2) functions of RECK in normal development and adult homeostasis, particularly in the vascular and central nervous systems, (3) search for chemicals upregulating RECK in cancer cells, (4) search for other molecules suppressing malignancy, and (5) the relationship between circadian rhythm and cancer. We organize Oncology Course (Graduate School) and take part in the educational programs such as Medical Science Research (Medical Science, Master), Molecular Cell Biology (2nd year, undergraduate), and Basic Chemical Experiments (elective course of the University). In the laboratory, graduate students and researchers with various backgrounds and nationalities enjoy their experiments aiming at solving the puzzles of their own choices, learning necessary knowledge and techniques in groups, and participating in active scientific discussions in cooperative atmosphere.
a. Isolation of transformation suppressor genes,b. Domains in RECK, c. Activities of RECK, d. Morphology of RECK dimer
Recent Publications1.Shi G, Yoshida Y, Yuki K, Nishimura T, Kawata Y, Kawashima M, Iwaisako K, Yoshikawa K, Kurebayashi J, Toi M, Noda M. Pattern of RECK CpG methylation as a potential marker for predicting breast cancer prognosis and drug-sensitivity. Oncotarget 7, 8620 (2016).
2.Almeida GM, Yamamoto M, Morioka Y, Ogawa S, Matsuzaki T, Noda M. Critical roles for murine Reck in the regulation of vascular patterning and stabilization. Sci Rep 5, 17860 (2015).
3.Yuki K, Yoshida Y, Inagaki R, Hiai H, Noda M. E-cadherin-downregulation and RECK-upregulation are coupled in the non-malignant epithelial cell line MCF10A but not in multiple carcinoma-derived cell lines. Sci Rep 4, 4568 (2014).
4.Yoshida Y, Ninomiya K, Hamada H, Noda M. Involvement of the SKP2-p27(KIP1) pathway in suppression of cancer cell proliferation by RECK. Oncogene 31, 4128-4138 (2012).
5.Yamamoto M, Matsuzaki T, Takahashi R, Adachi E, Maeda Y, Yamaguchi S, Kitayama H, Echizenya M, Morioka Y, Alexander DB, Yagi T, Itohara S, Nakamura T, Akiyama H, Noda M. The transformation suppressor gene Reck is required for postaxial patterning in mouse forelimbs. Biol Open 1, 458-466 (2012).
Molecular OncologyProfessor: Makoto Noda
Associate professor: Hitoshi Kitayama
Assistant professor: Tomoko Matsuzaki
Specific Assistant Professor: Takao Miki