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Oncogenic RAS Regulates Long Noncoding RNA Orilnc1 in Human Cancer.

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机构： [1]Department of Gynecology and Obstetrics, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China. [2]Center for Research on Reproduction & Women's Health, Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. [3]Key Laboratory of Birth Defects and Related Disease of Women and Children, Sichuan University, Ministry of Education, Chengdu, Sichuan, China. [4]Melanoma Research Center, Wistar Institute, Philadelphia, Pennsylvania. [5]Molecular and Cellular Oncogenesis Program, Wistar Institute, Philadelphia, Pennsylvania. [6]Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. [7]Department of Computer Science, New Jersey Institute of Technology, Newark, New Jersey. [8]Department of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, Texas. [9]Massachusetts General Hospital Cancer Center, Boston, Massachusetts. [10]Center for Stem Biology and Tissue Engineering, Department of Biology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China. [11]Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

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RAS and its downstream cascades transmit cellular signals, resulting in increased transcription of genes involved in cell growth and division. Protein-coding gene targets of RAS signaling have been characterized extensively, but long noncoding RNAs (lncRNA) regulated by these processes have not. Using a custom-designed lncRNA microarray, we identified the lncRNA Orilnc1 as a genetic target of RAS that is critical for RAS oncogenicity. Orilnc1 expression was regulated by RAS-RAF-MEK-ERK signaling via the transcription factor AP1. Orilnc1 was highly expressed in BRAF-mutant cancers, such as melanoma. Silencing of Orilnc1 blocked tumor cell proliferation and growth in vitro and in vivo In addition, Orilnc1 blockade reduced expression of cyclin E1 and induced G1-S cell-cycle arrest in tumor cells. Taken together, our results identify Orilnc1 as a novel, nonprotein mediator of RAS/RAF activation that may serve as a therapeutic target in RAS/RAF-driven cancers. Cancer Res; 77(14); 3745-57. ©2017 AACR. ©2017 American Association for Cancer Research.

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出版当年[2017]版：

大类 | 1 区

医学

小类 | 1 区肿瘤学

最新[2023]版：

大类 | 1 区

医学

小类 | 2 区肿瘤学

第一作者：

第一作者机构： [1]Department of Gynecology and Obstetrics, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China. [2]Center for Research on Reproduction & Women's Health, Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. [3]Key Laboratory of Birth Defects and Related Disease of Women and Children, Sichuan University, Ministry of Education, Chengdu, Sichuan, China.

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通讯作者：

通讯机构： [2]Center for Research on Reproduction & Women's Health, Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. [4]Melanoma Research Center, Wistar Institute, Philadelphia, Pennsylvania. [5]Molecular and Cellular Oncogenesis Program, Wistar Institute, Philadelphia, Pennsylvania. [*1]University of Pennsylvania, 1207 BRB II/III,Philadelphia, PA 19104. [*2]The Wistar Institute, 3601 Spruce Street, Room 472, Philadelphia, PA 19104.

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