Kyushu University Academic Staff Educational and Research Activities Database
List of Books
Kiyoko Kato Last modified date:2022.06.16

Professor / Reproductive and Developmental Medicine / Department of Clinical Medicine / Faculty of Medical Sciences

1. Yagi H, Kato K, Chapter5; The Role of G Protein-Coupled Receptor Signaling in Gynecologic Malignancy
Molecular Diagnosis and Targeting for Gynecologic Malignancy
, Springer, 10.1007/978-981-33-6013-6, 57-70, 2021.03, G protein-coupled receptors(GPCRs) are seven transmembrane receptors that represent the family of cell surface receptors. Ligand binding induces conformational changes in GPCRs, which lead to the activation of their associated heterotrimeric G proteins. GPCR signaling regulates diverse biological functions, including cell proliferation, migration, and angiogenesis. Cancer cells can co-opt the activity of GPCR signaling to proliferate autonomously, evade immune detection, increase their nutrient and oxygen supply, invade their surrounding tissues, and metastasize to other organs, Dysregulation of GPCR signaling, induced by elevated expression of GPCRs, G proteins, or their ligands as well as activating mutations of these genes, contributes to the progression of various human cancers. Although GPCRs are associated with cancer progression and represent one of the most druggable molecules, there are relatively few cancer treatments targeting these receptors. Therefore, by better understanding the molecular mechanisms underlying GPCR function in cancer, we can identify novel strategies for cancer diagnosis, prevention, and treatment. We present here our current understanding of many roles of GPCR signaling in the progression of gynecologic malignancy and the potential benefits of targeting GPCRs and signaling circuits in cancer treatment.
Keywords GPCR・G protein・Mutation・Inflammation・Angiogenesis Metastasis・LPA.
2. Kiyoko Kato, Pathogenesis of endometrial cancer
Current Approaches to Endometrial Cancer.
, Future Medicine, 18-32, 2014.11.
3. Kato K and Wake N, Contribution of estrogen receptor α and progesterone receptor-B to oncogenic K-Ras-mediated NIH3T3 cell transformation.:Cell and Molecular Biology of Endometrial Carcinoma, Springer-Verlag Tokyo, 207-218, 2003.01.