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PGE2-JNK signaling axis non-canonically promotes Gli activation by protecting Gli2 from ubiquitin-proteasomal degradation

文献类型：期刊论文

作者Yang, Jun1; Wang, Juan1; Liu, Yuan1; Zhang, Yu1; Huang, Wenjing1; Zou, Yu2,3; Qiu, Yanyan2,3; Cai, Weiyang4; Gao, Jing5,6; Zhou, Hu5,6
刊名CELL DEATH & DISEASE
出版日期2021-07-15
卷号12期号:7页码:10
ISSN号2041-4889
DOI10.1038/s41419-021-03995-z
通讯作者Yin, Pei-hao(yinpeihao1975@hotmail.com) ; Tan, Wenfu(wftan@fudan.edu.cn)
英文摘要Both bench and bedside investigations have challenged the supportive role of Hedgehog (Hh) activity in the progression of colorectal cancers, thus raising a critical need to further deeply determine the contribution of Hh to the growth of colorectal cancer. Combining multiple complementary means, including in vitro and in vivo inflammatory colorectal cancer models, and pathological analysis of clinical colorectal cancer patients samples. We report that colorectal cancer cells hijack prostaglandin E2 (PGE2) to non-canonically promote Hh transcriptional factor Gli activity and Gli-dependent proliferation of colorectal cancer cells in a Smo-independent manner. Mechanistically, PGE2 activates c-Jun N-terminal kinase (JNK), which in turn enables Gli2 to evade ubiquitin-proteasomal degradation by phosphorylating Gli2 at Thr1546. This study not only presents evidence for understanding the contribution of Hh to colorectal cancers, but also provides a novel molecular portrait underlying how PGE2-activated JNK fine-tunes the evasion of Gli2 from ubiquitin-proteasomal degradation. Therefore, it proposes a rationale for the future evaluation of chemopreventive and selective therapeutic strategies for colorectal cancers by targeting PGE2-JNK-Gli signaling route.
WOS关键词MULTIPLE INTESTINAL NEOPLASIA ; HEDGEHOG PATHWAY ; TUMOR-GROWTH ; CELL GROWTH ; CANCER ; PHOSPHORYLATION ; TRANSDUCTION ; INFLAMMATION ; REQUIREMENT ; DOWNSTREAM
资助项目National Natural Science Foundation of China[81341136] ; National Natural Science Foundation of China[81573452] ; National Natural Science Foundation of China[81672354] ; National Natural Science Foundation of China[81773767] ; ''twelfth five year key subject (Integrated Chinese and Western Medicine) of State Administration of Traditional Chinese medicine ; Academic leader candidate of 315 Health and family planning commission System Project in Putuo District, Shanghai[14Q-RC-08] ; Xinglin Scholar of Shanghai University of Traditional Chinese Medicine[B-X-72]
WOS研究方向Cell Biology
语种英语
WOS记录号WOS:000675639700002
出版者SPRINGERNATURE
源URL[http://119.78.100.183/handle/2S10ELR8/296784]  
专题中国科学院上海药物研究所
通讯作者Yin, Pei-hao; Tan, Wenfu
作者单位1.Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China
2.Shanghai Univ Tradit Chinese Med, Putuo Hosp, Dept Gen Surg, Shanghai 200062, Peoples R China
3.Anhui Med Univ, Shanghai Putuo Cent Sch Clin Med, Dept Gen Surg, Hefei 230601, Anhui, Peoples R China
4.Shanghai Jiao Tong Univ, Sch Med, Shanghai Pepoples Hosp 9, Dept Oncol, 280 Mohe Rd, Shanghai 201999, Peoples R China
5.Chinese Acad Sci, Shanghai Inst Mat Med, Dept Analyt Chem, Shanghai 201203, Peoples R China
6.Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China
7.Shanghai Jiao Tong Univ, Key Lab Cell Differentiat & Apoptosis,Sch Med, Shanghai Univ E Inst,Chinese Minist Educ,Hongqiao, Shanghai Tongren Hosp,Fac Basic Med,Chem Biol Div, Shanghai, Peoples R China
8.Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63108 USA
9.Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA
推荐引用方式
GB/T 7714		 Yang, Jun,Wang, Juan,Liu, Yuan,et al. PGE2-JNK signaling axis non-canonically promotes Gli activation by protecting Gli2 from ubiquitin-proteasomal degradation[J]. CELL DEATH & DISEASE,2021,12(7):10.
APA Yang, Jun.,Wang, Juan.,Liu, Yuan.,Zhang, Yu.,Huang, Wenjing.,...&Tan, Wenfu.(2021).PGE2-JNK signaling axis non-canonically promotes Gli activation by protecting Gli2 from ubiquitin-proteasomal degradation.CELL DEATH & DISEASE,12(7),10.
MLA Yang, Jun,et al."PGE2-JNK signaling axis non-canonically promotes Gli activation by protecting Gli2 from ubiquitin-proteasomal degradation".CELL DEATH & DISEASE 12.7(2021):10.

入库方式： OAI收割

来源：上海药物研究所

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