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- W4313257037 abstract "Hedgehog (Hh) signaling pathway includes canonical and non-canonical activation manners. In colorectal cancer, we have previously shown that PGE2-JNK could initiate non-canonical activation of the Hh signaling pathway. In this study, we showed that c-Jun, a classic substrate of JNK, increased Gli2 protein stability after phosphorylated by PGE2. Suppressing the function of c-Jun or JNK indicated that c-Jun prevents Gli2 from protease degradation caused by PGE2-JNK. Moreoer, we revealed that less ubiquitination of Gli2 was detected in colorectal cancer cells treated with PGE2 while suppression of c-Jun restored the ubiquitination of Gli2. In addition, we observed that suppression of c-Jun significantly decreased Gli2 expression no matter when Gli2 remained in phosphorylation or non-phosphorylation state. These phenomena were recapitulated, when the endpoint of Gli2 expression was replaced by Gli2 ubiquitination. Furthermore, we demonstrated that restricting c-Jun function ablated the PGE2-provoked Hh activity and proliferation of colorectal cancer cells. These results elucidated that the evasion of Gli2 with phosphorylation from proteasomal-ubiquitin degradation needed the cooperation of phosphorylated c-Jun by kinase JNK, which contributed to promoting Hh activation and the proliferation of colorectal cancer cells. This study provides a theoretical foundation to target PGE2 downstream for the prevention and treatment of colorectal cancer." @default.
- W4313257037 created "2023-01-06" @default.
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- W4313257037 date "2023-03-01" @default.
- W4313257037 modified "2023-09-27" @default.
- W4313257037 title "c-Jun phosphorylated by JNK is required for protecting Gli2 from proteasomal-ubiquitin degradation by PGE2-JNK signaling axis" @default.
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- W4313257037 doi "https://doi.org/10.1016/j.bbamcr.2022.119418" @default.
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