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Kohei Otsubo Last modified date：2024.04.09

Assistant Professor / Department of Clinical Medicine
Faculty of Medical Sciences


Other Organization
Research Institute for Deseases of the Chest


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Homepage
https://kyushu-u.elsevierpure.com/en/persons/kohei-otsubo
　Reseacher Profiling Tool　Kyushu University Pure
Academic Degree
Ph.D in Medicine
Country of degree conferring institution (Overseas)
No
Field of Specialization
Medical Oncology
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Development of treatment for lung cancer for lung cancer with interstitial pneumonia
    keyword : Lung cancer, Interstitial pneumonia
    2017.04～2021.03.
  • Functional analysis of Hippo pathway-related genes in the lung cancer
    keyword : Hippo pathway, Lung cancer
    2017.04～2020.03.
  • Development of treatment for lung cancer targeting cancer stem cells.
    keyword : Lung cancer, Cancer stem cell
    2014.04～2017.03.
  • Functional analysis of Hippo pathway-related genes in the lung
    keyword : Hippo pathway, Lung
    2011.04～2017.03.
Academic Activities
Papers
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1. Otsubo K, Nosaki K, Imamura CK, Ogata H, Fujita A, Sakata S, Hirai F, Toyokawa G, Iwama E, Harada T, Seto T, Takenoyama M, Ozeki T, Mushiroda T, Inada M, Kishimoto J, Tsuchihashi K, Suina K, Nagano O, Saya H, Nakanishi Y, Okamoto I, Phase I study of salazosulfapyridine in combination with cisplatin and pemetrexed for advanced non-small-cell lung cancer, Cancer Science, 108, 1843-1849, 2017.09.
2. Otsubo K, Goto H, Nishio M, Kawamura K, Yanagi S, Nishie W, Sasaki T, Maehama T, Nishina H, Mimori K, Nakano T, Shimizu H, Mak TW, Nakao K, Nakanishi Y, Suzuki A, MOB1-YAP1/TAZ-NKX2.1 axis controls bronchioalveolar cell differentiation, adhesion and tumour formation., Oncogene, 2017.03, Mps One Binder Kinase Activator (MOB)1A/1B are core components of the Hippo pathway. These proteins, which coactivate LArge Tumor Suppressor homolog (LATS) kinases, are also tumor suppressors. To investigate MOB1A/B’s roles in normal physiology and lung cancer, we generated doxycycline (Dox)-inducible, bronchioalveolar epithelium–specific, null mutations of MOB1A/B in mice [SPC-rtTA/(tetO)7-Cre/Mob1aflox/flox/Mob1b-/-; termed luMob1DKO) mice]. Most mutants (70%) receiving Dox in utero [luMob1DKO (E6.5-18.5) mice] died of hypoxia within 1hr post-birth. Their alveolar epithelial cells showed increased proliferation, impaired YAP1/TAZ-dependent differentiation, and decreased surfactant protein production, all features characteristic of human respiratory distress syndrome　(RDS). Intriguingly, mutant mice that received Dox postnatally [luMob1DKO (P21–41) mice] did not develop spontaneous lung adenocarcinomas, and urethane treatment-induced lung tumor formation was decreased (rather than increased). Lungs of luMob1DKO (P21–41) mice exhibited increased detachment of bronchiolar epithelial cells and decreased numbers of the bronchioalveolar stem cells (BASCs) thought to initiate lung adenocarcinomas. YAP1/TAZ-NKX2.1-dependent expression of collagen XVII, a key hemidesmosome component, was also reduced. Thus, a MOB1-YAP1/TAZ-NKX2.1 axis is essential for normal lung homeostasis and expression of the collagen XVII protein necessary for alveolar stem cell maintenance in the lung niche..


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