The LINC01138 drives malignancies via activating arginine methyltransferase 5 in hepatocellular carcinoma

Zhe Li, Jiwei Zhang, Xinyang Liu, Shengli Li, Qifeng Wang, Di Chen, Zhixiang Hu, Tao Yu, Jie Ding, Jinjun Li, Ming Yao, Jia Fan, Shenglin Huang, Qiang Gao (), Yingjun Zhao () and Xianghuo He ()
Additional contact information
Zhe Li: Shanghai Medical College, Fudan University
Jiwei Zhang: Shanghai Medical College, Fudan University
Xinyang Liu: Shanghai Medical College, Fudan University
Shengli Li: Shanghai Medical College, Fudan University
Qifeng Wang: Shanghai Medical College, Fudan University
Di Chen: Shanghai Medical College, Fudan University
Zhixiang Hu: Shanghai Medical College, Fudan University
Tao Yu: Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine
Jie Ding: Shanghai Medical College, Fudan University
Jinjun Li: Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine
Ming Yao: Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine
Jia Fan: Shanghai Medical College, Fudan University
Shenglin Huang: Shanghai Medical College, Fudan University
Qiang Gao: Shanghai Medical College, Fudan University
Yingjun Zhao: Shanghai Medical College, Fudan University
Xianghuo He: Shanghai Medical College, Fudan University

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Recurrent chromosomal aberrations have led to the discovery of oncogenes or tumour suppressors involved in carcinogenesis. Here we characterized an oncogenic long intergenic non-coding RNA in the frequent DNA-gain regions in hepatocellular carcinoma (HCC), LINC01138 (long intergenic non-coding RNA located on 1q21.2). The LINC01138 locus is frequently amplified in HCC; the LINC01138 transcript is stabilized by insulin like growth factor-2 mRNA-binding proteins 1/3 (IGF2BP1/IGF2BP3) and is associated with the malignant features and poor outcomes of HCC patients. LINC01138 acts as an oncogenic driver that promotes cell proliferation, tumorigenicity, tumour invasion and metastasis by physically interacting with arginine methyltransferase 5 (PRMT5) and enhancing its protein stability by blocking ubiquitin/proteasome-dependent degradation in HCC. The discovery of LINC01138, a promising prognostic indicator, provides insight into the molecular pathogenesis of HCC, and the LINC01138/PRMT5 axis is an ideal therapeutic target for HCC treatment.

Date: 2018
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DOI: 10.1038/s41467-018-04006-0

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