Basic Medicine, Oncology
Cancer Molecular Biology(Miyagi Cancer Center)
Diagnostic and Therapeutic Approaches by Targeting the Inherent Nature of Cancer Cells
Medical Sciences Course
- Master / Doctoral Degree
- SHIMA, Hiroshi
Professor, M.D. Ph.D.
shima*med.tohoku.ac.jp (Please convert "*" into "@".)
- Development of diagnostic and therapeutic approaches by targeting the metabolic disorder of cancer cells
- Development of diagnostic and therapeutic modalities for cancer by targeting kinases and phosphatases
Warburg effect, Protein phosphatase, genetic instability
genetically engineered mice, live imaging, metabolic analysis
(1) There are fundamental differences in the metabolic pathways operating in malignant tissue. Cancer cells preferentially convert glucose into lactate even when oxygen level are not limiting, a process termed “aerobic glycolysis” or the Warburg Effect. Our project is that to develop therapy by targeting the metabolic disorder of cancer cells.
(2) The phosphorylation status of proteins is regulated by the balance of kinase and phosphatase activities. Studies into the causes of abnormal phosphorylation have, until now, mainly been focused on kinases. Many kinase inhibitors have been applied as a molecular targeted therapy. At the same time, numerous mechanisms which regulate phosphatase activities have been identified, and their dysfunction to be related to various diseases. We are trying to develop diagnostic and therapeutic modalities for cancer by targeting kinases and phosphatases.
- Matsuda S, et al. Nuclear pyruvate kinase M2 complex serves as a transcriptional coactivator of arylhydrocarbon receptor. Nucleic Acids Res 44(22):636-47, 2016
- Ogoh H, et al. The protein phosphatase 6 catalytic subunit (Ppp6c) is indispensable for proper post-implantation embryogenesis. Mech. Dev. 139:1-9, 2016
- Hayashi K, et al. Abrogation of protein phosphatase 6 promotes skin carcinogenesis induced by DMBA. Oncogene 34(35):4647-75, 2015
- Kato H, et al. Loss of protein phosphatase 6 in mouse keratinocytes increases susceptibility to ultraviolet-B-induced carcinogenesis. Cancer Lett. 365(2):223-8, 2015
- Konno M, et al. Embryonic MicroRNA-369 Controls Metabolic Splicing Factors and Urges Cellular Reprograming. PLos One 10 (7);e132789, 2015
- Takahashi K et al. Sialidase NEU3 contributes neoplastic potential on colon cancer cells as a key modulator of gangliosides by regulating Wnt signaling. Int J Cancer 137(7):1560-73, 2015