Publication Date:
2019
Description:
〈sec〉〈st〉Synopsis〈/st〉〈p〉〈textbox textbox-type="graphic"〉〈p〉〈inline-fig〉〈/inline-fig〉〈/p〉〈/textbox〉〈/p〉
〈p〉Pathogenesis of pancreatic ductal cancer (PDAC) is driven by the recurrent oncogenic Kras〈sup〉G12D〈/sup〉 mutation. Here, genetic findings uncover the homeodomain protein TG-interacting factor 1 (TGIF1) to be inactivated by phosphorylation orchestrated by constitutive Kras, providing new insights into biphasic roles of TGF-β signaling during PDAD initiation and progression. A video of this synopsis is available online at 〈a href="http://www.embopress.org/video_EMBOJ_2018_101067"〉http://www.embopress.org/video_EMBOJ_2018_101067〈/a〉.〈/p〉
〈p〉 〈l type="unord"〉〈li〉〈p〉TGIF1 is dispensable for normal pancreatic development.〈/p〉〈/li〉
〈li〉〈p〉Pancreas-specific 〈i〉Tgif1〈/i〉 inactivation accelerates Kras〈sup〉G12D〈/sup〉-driven tumorigenesis and metastasis in mice.〈/p〉〈/li〉
〈li〉〈p〉TGIF1 restricts PDAC through repression of Twist1 expression and activity.〈/p〉〈/li〉
〈li〉〈p〉Phosphorylation of TGIF1 by constitutive Kras〈sup〉G12D〈/sup〉/MAPK signaling disrupts its tumor suppressor function in human PDAC.〈/p〉〈/li〉〈/l〉 〈/p〉〈/sec〉
Print ISSN:
0261-4189
Electronic ISSN:
1460-2075
Topics:
Biology
,
Medicine
