GNAI1 and GNAI3 reduce colitis-associated tumorigenesis in mice by blocking IL6 signaling and down-regulating expression of GNAI2

Abstract: Interleukin 6 (IL6) and tumor necrosis factor contribute to the development of colitis-associated cancer (CAC). We investigated these signaling pathways and the involvement of G protein subunit alpha i1 (GNAI1), GNAI2, and GNAI3 in the development of CAC in mice and humans. GNAI1;3 suppres...

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Autores principales: Li, Zhi-Wei, Sun, Beicheng, Gong, Ting, Guo, Sheng, Zhang, Jianhua, Wang, Junlong, Sugawara, Atsushi, Jiang, Meisheng, Yan, Junjun, Gurary, Alexandra, Zheng, Xin, Gao, Bifeng, Xiao, Shu-Yuan, Chen, Wenlian, Ma, Chi, Farrar, Christine, Zhu, Chenjun, Chan, Owen T. M., Xin, Can, Winnicki, Andrew, Winnicki, John, Tang, Mingxin, Park, Ryan, Winnicki, Mary, Diener, Katrina, Wang, Zhanwei, Liu, Qicai, Chu, Catherine H., Arter, Zhaohui L., Yue, Peibin, Alpert, Lindsay, Hui, George S., Fei, Peiwen, Turkson, James, Yang, Wentian, Wu, Guangyu, Tao, Ailin, Ramos, Joe W., Moisyadi, Stefan, Holcombe, Randall F., Jia, Wei, Birnbaumer, Lutz, Zhou, Xiqiao, Chu, Wen-Ming
Formato: Artículo
Lenguaje:Inglés
Publicado: Elsevier 2019
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Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/9271
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Sumario:Abstract: Interleukin 6 (IL6) and tumor necrosis factor contribute to the development of colitis-associated cancer (CAC). We investigated these signaling pathways and the involvement of G protein subunit alpha i1 (GNAI1), GNAI2, and GNAI3 in the development of CAC in mice and humans. GNAI1;3 suppresses DSS-plus-AOM–induced colon tumor development in mice, whereas expression of GNAI2 in CD11c+ cells and IL6 in CD4+/CD11b+ DCs appears to promote these effects. Strategies to induce GNAI1;3, or block GNAI2 and IL6, might be developed for the prevention or therapy of CAC in patients.