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Título : | GNAI1 and GNAI3 reduce colitis-associated tumorigenesis in mice by blocking IL6 signaling and down-regulating expression of GNAI2 | Autor : | 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 |
Palabras clave : | CANCER; TUMORES; COLITIS; CARCINOGENESIS | Fecha de publicación : | 2019 | Editorial : | Elsevier | Cita : | Li, Z. et al. GNAI1 and GNAI3 reduce colitis-associated tumorigenesis in mice by blocking IL6 signaling and down-regulating expression of GNAI2 [en línea]. Gastroenterology. 2019, 156(8). doi:10.1053/j.gastro.2019.02.040 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/9271 | Resumen : | 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. | URI : | https://repositorio.uca.edu.ar/handle/123456789/9271 | ISSN : | 0016-5085 | Disciplina: | MEDICINA | DOI: | 10.1053/j.gastro.2019.02.040 | Derechos: | Acceso abierto |
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