LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway
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Lihui Liu1,2,3,*, Haiyan Yue1,2,3,*, Qinghua Liu1,2,*, Jiao Yuan1,2,*, Jing Li4, Guifeng Wei1,2, Xiaomin Chen1,2, Youyong Lu5, Mingzhou Guo6, Jianjun Luo1,2, Runsheng Chen1,2,7
1Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
2Beijing Key Laboratory of Noncoding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
3Graduate School of Chinese Academy of Sciences, Beijing 100049, China
4Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College Hospital, Center of Excellence in Tissue Engineering, School of Basic Medicine, Peking Union Medical College, Beijing 100005, China
5Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing 100142, China
6Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing 100853, China
7Research Network of Computational Biology, RNCB, Beijing 100101, China
*These authors contributed equally to this work
Runsheng Chen, e-mail: email@example.com
Jianjun Luo, e-mail: firstname.lastname@example.org
Keywords: long noncoding RNAs, MT1JP, TIAR, p53, tumor suppressor
Received: September 09, 2015 Accepted: February 05, 2016 Published: February 19, 2016
Accumulating evidence suggests that long noncoding RNAs (lncRNAs) play important roles in transcriptional regulation, whereas the extent to which the lncRNAs also function at the posttranscriptional level is less known. In the present study, we report a lncRNA named MT1JP which acts as a tumor suppressor through a posttranscriptional mechanism. We found that MT1JP is differentially expressed in tumor tissues by analyzing data from a customized microarray applied to 76 pairs of matched normal and cancer tissue samples. By associating with the RNA-binding protein TIAR, MT1JP enhanced the translation of the master transcription factor p53, thereby regulating a series of pathways involving p53, such as the cell cycle, apoptosis and proliferation. When MT1JP was down-regulated, the protein level of p53 declined, which in turn accelerated cell deterioration and tumor formation. Moreover, differential expression of MT1JP in cancerous and normal tissues suggests that it may be a promising prognostic marker and a therapeutic target. Taken together, we identified MT1JP as a critical factor in restraining cell transformation by modulating p53 translation through interactions with TIAR, and this finding is likely to shed new light on future investigations about posttranscriptional or translational effects of lncRNAs during cell transformation.
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