Department of Developmental Biology and Neurosciences
Division of Developmental Regulation

Cancer Biology 分野

Yuki Yoshino
キャンパス Seiryo キャンパス
専攻分野 Molecular oncology
連絡先 022-717-8478

I studied on molecular mechanisms of oncogenesis and malignancy. I also studied on anticancer effects of molecular targeted drugs
and resistance to chemotherapy in several malignant neoplasms including pancreatic, colorectal, breast and lung cancers. Now, I am interested in regulatory mechanisms of cell division because disruption of the regulation will result in the chromosomal instability and, ultimately, cancer.

経歴 2009 March Graduated from the School of Medicine, Tohoku 2009 April Clinical junior resident of Tohoku University 2015 March Finished the doctoral course in the Graduate School of Medicine, Tohoku University 2015 April Post-Doc at the Department of Cancer Biology, IDAC, Tohoku University 2015 September Assistant Professor at the Department of Cancer Biology, IDAC, Tohoku University
  1. Yoshino Y, Chikashi I. Inhibition of glycogen synthase kinase-3 beta induces apoptosis and mitotic catastrophe by disrupting centrosome regulation in cancer cells. Sci. Rep. 2015 vol. 5 13249
  2. Fujita H, Yoshino Y, Chiba N. Regulation of centrosome cycle. Mol. Cell. Oncol 2015 in press
  3. Yoshino Y, Suzuki M, Takahashi H, Ishioka C. Inhibition of invasion by glycogen synthase kinase-3 beta inhibitors through dysregulation of actin re-organisation via down-regulation of WAVE2. Biochem. Biophys. Res. Commun. 2015. Vol. 464, pp 275-280
  4. Yoshino Y, Akiyama S, Ouchi K, Oishi T, Takahashi H, Lee J, Takahashi S, Shimodaira H, Kato S, Ishioka C. Acute exacerbation of paraneoplastic neurological syndrome after massive tumor lysis of neuroendocrine carcinoma by chemoradiotherapy. Int. Cancer Conf. J. 2013. vol. 2, pp 247-250
  5. Sekine H, Chen N, Sato K, Saiki Y, Yoshino Y, Umetsu Y, Jin G, Nagase H, Gu Z, Fukushige S, Sunamura M, Horii A. S100A4, frequently overexpressed in various human cancers, accelerates cell motility in pancreatic cancer cells. Biochem. Biophys. Res. Commun. 2012. vol. 429, pp 214-219
  6. Saiki Y*, Yoshino Y*, Fujimura H*, Manabe T, Kudo Y, Shimada M, Mano N, Nakano T, Lee Y, Shimizu S, Oba S, Fujiwara S, Shimizu H, Chen N, Nezhad ZK, Jin G, Fukushige S, Sunamura M, Ishida M, Motoi F, Egawa S, Unno M, Horii A (* co-first author) DCK is frequently inactivated in acquired gemcitabine-resistant human cancer cells. Biochem. Biophys. Res. Commun. 2012. vol. 421, pp 98-104
  7. Yoshino Y, Ishida M, Horii A. A new 10-min ligation method using a modified buffer system with a very low amount of T4 DNA ligase: the “Coffee Break Ligation” technique. Biotechnol. lett. 2007. vol. 29, pp 1557–60
所属学会 <p>The Japanese Society of Internal Medicine, Japanese Cancer Association, Japan Society of Clinical Oncology, Japanese Society of Medical Oncology</p>


Cancer is a result of accumulated genomic aberration. In addition to alteration in DNA sequence and epigenetic modification, abnormalities of chromosome number and structure are also related with oncogenesis. I have studied on regulatory mechanisms of centrosome, which is essential organelle in accurate cell division. It also interest me how cancer with chromosomal instability survive elimination machinery of many checkpoints. Finally, I aim for development of a new class of chemotherapeutic drugs which targets the cell division machinery.


Disruption of cellular regulatory mechanisms make cells to be malignant. Cancer cells depend their survival on the dysregulated but somewhat workable regulatory machineries. Such injured machineries will be good targets of therapeutic intervention. Although, to develop such new therapeutic strategies, we must know how normal cells deal with a complex event of cell division and how cancer cells survive disruption of these essential mechanisms. These are very interesting and exciting problems. Let’s study on the cancer biology with us.