YAP1 is a potent driver of the onset and progression of oral squamous cell carcinoma
Hirofumi Omori(Kyushu University), Miki Nishio(Kobe University), Muneyuki Masuda(National Hospital Organization Kyushu Cancer Center), Yosuke Miyachi(Kobe University), Fumihito Ueda(Kobe University), Takafumi Nakano(National Hospital Organization Kyushu Cancer Center), Kuniaki Sato(Kyushu University), Koshi Mimori(Kyushu University Beppu Hospital), Kenichi Taguchi(National Hospital Organization Kyushu Cancer Center), Hiroki Hikasa(University of Occupational and Environmental Health Japan), Hiroshi Nishina(Tokyo Medical and Dental University), Hironori Tashiro(Kumamoto Health Science University), Tohru Kiyono(Genesis Research Institute), Tak W. Mak(University Health Network), Kazuwa Nakao(Kyoto University), Takashi Nakagawa(Kyushu University), Tomohiko Maehama(Kobe University), Akira Suzuki(Kyushu University)
Cited by 118Open Access
Abstract
and thus endogenous YAP1 hyperactivation underwent surprisingly rapid and highly reproducible tumorigenesis, developing tongue carcinoma in situ within 2 weeks and invasive SCC within 4 weeks. In humans, precancerous tongue dysplasia displays YAP1 activation correlating with reduced patient survival. Combinations of molecules mutated in OSCC may increase and sustain YAP1 activation to the point of oncogenicity. Strikingly, siRNA or pharmacological inhibition of YAP1 blocks murine OSCC onset in vitro and in vivo. Our work justifies targeting YAP1 as therapy for OSCC and perhaps HNSCC, and our mouse model represents a powerful tool for evaluating these agents.
Related Papers
No related papers found
Powered by citation graph analysis