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YAP-IL-6ST autoregulatory loop activated on APC loss controls colonic tumorigenesis

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机构： [1]Univ Calif San Diego, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA; [2]Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA; [3]Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA; [4]Kyushu Univ, Grad Sch Med Sci, Dept Surg & Sci, Fukuoka 8128582, Japan; [5]Keio Univ, Sch Med, Dept Microbiol & Immunol, Tokyo 1608582, Japan; [6]Univ Calif San Diego, Moores Canc Ctr, Dept Pharmacol, La Jolla, CA 92093 USA; [7]Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA; [8]NCI, Sanford Burnham Prebys Med Discovery Inst, Designated Canc Ctr, La Jolla, CA 92037 USA; [9]Univ Calif San Diego, Inst Genom Med, La Jolla, CA 92093 USA; [10]German Canc Consortium, D-69120 Heidelberg, Germany; [11]Georg Speyer Haus, Inst Tumor Biol & Expt Therapy, D-60596 Frankfurt, Germany; [12]German Canc Res Ctr, D-69120 Heidelberg, Germany; [13]Sun Yat Sen Univ, Ctr Canc, Collaborat Innovat Ctr Canc Med, State Key Lab Oncol, Guangzhou 510060, Guangdong, Peoples R China; [14]Med Univ Graz, Inst Pathol, A-8036 Graz, Austria; [15]Univ Connecticut, Ctr Hlth, Sch Med, Dept Immunol, Farmington, CT USA; [16]Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA; [17]Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI 48109 USA; [18]Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA; [19]Med Univ Vienna, Clin Inst Pathol, A-1090 Vienna, Austria; [20]Med Univ Vienna, Ludwig Boltzmann Inst Canc Res, A-1090 Vienna, Austria; [21]Univ Vet Med Vienna, Dept Pathol Lab Anim, A-1210 Vienna, Austria; [22]Otto von Guericke Univ, Dept Pathol, D-39120 Magdeburg, Germany; [23]Paracelsus Private Univ Salzburg, Teaching Hosp, Hosp Oberndorf, Dept Internal Med, A-5110 Oberndorf, Austria; [24]Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA

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关键词： colorectal cancer adenomatous polyposis coli IL-6ST/gp130 YAP STAT3

摘要：

Loss of tumor suppressor adenomatous polyposis coli (APC) activates beta-catenin to initiate colorectal tumorigenesis. However, beta-catenin (CTNNB1) activating mutations rarely occur in human colorectal cancer (CRC). We found that APC loss also results in up-regulation of IL-6 signal transducer (IL-6ST/gp130), thereby activating Src family kinases (SFKs), YAP, and STAT3, which are simultaneously up-regulated in the majority of human CRC. Although, initial YAP activation, which stimulates IL6ST gene transcription, may be caused by reduced serine phosphorylation, sustained YAP activation depends on tyrosine phosphorylation by SFKs, whose inhibition, along with STAT3-activating JAK kinases, causes regression of established colorectal tumors. These results explain why APC loss is a more potent initiating event than the mere activation of CTNNB1.

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出版当年[2017]版：

大类 | 1 区

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最新[2023]版：

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小类 | 1 区综合性期刊

第一作者：

第一作者机构： [1]Univ Calif San Diego, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA; [2]Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA; [3]Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA; [4]Kyushu Univ, Grad Sch Med Sci, Dept Surg & Sci, Fukuoka 8128582, Japan; [5]Keio Univ, Sch Med, Dept Microbiol & Immunol, Tokyo 1608582, Japan;

通讯作者：

通讯机构： [1]Univ Calif San Diego, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA; [2]Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA; [3]Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA; [24]Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA

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