Inhibition of c‐Jun NH2‐terminal kinase switches Smad3 signaling from oncogenesis to tumor‐ suppression in rat hepatocellular carcinoma
Hiromitsu Nagata, Etsuro Hatano, Masaharu Tada, Miki Murata, Koji Kitamura, Hiroyuki Asechi, Masato Narita, Atsuko Yanagida, Nobuyuki Tamaki, Shintaro Yagi, Iwao Ikai, Koichi Matsuzaki, Shinji Uemoto – 28 May 2009 – Transforming growth factor beta (TGF‐β) signaling involves both tumor‐suppression and oncogenesis. TGF‐β activates the TGF‐β type I receptor (TβRI) and c‐Jun N‐terminal kinase (JNK), which differentially phosphorylate the mediator Smad3 to become COOH‐terminally phosphorylated Smad3 (pSmad3C) and linker‐phosphorylated Smad3 (pSmad3L).