Evidence map›Paper›PMID 26909858›Full record

ArticleOncotarget2016

LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway.

Lihui Liu, Haiyan Yue, Qinghua Liu, Jiao Yuan, Jing Li, Guifeng Wei, Xiaomin Chen, Youyong Lu, Mingzhou Guo, Jianjun Luo and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 114 citations in OpenAlex.

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  12. Epigenetic regulation of gastrointestinal cancers mediated by long non-coding RNAs.Cancer biomarkers : section A of Disease markers · 2022
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  13. Long Non-coding RNAs, LncSub-cellular biochemistry · 2022
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  14. Article
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  17. eLife · 2021
    Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 1 country.

Lihui LiuKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Haiyan YueKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Qinghua LiuKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Jiao YuanKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Jing LiInstitute 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.
Guifeng WeiKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Xiaomin ChenKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Youyong LuLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing 100142, China.
Mingzhou GuoDepartment of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing 100853, China.
Jianjun LuoKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Runsheng ChenKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Chinese Academy of Sciences · CNInstitute of Biophysics · CNChinese PLA General Hospital · CNPeking Union Medical College Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Cell Line, TumorCell Transformation, NeoplasticGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansNeoplasmsRNA-Binding ProteinsRNA, Long NoncodingSignal TransductionTumor Suppressor Protein p53RNA-Binding ProteinsRNA, Long NoncodingTIAL1 protein, humanTumor Suppressor Protein p53long noncoding RNAsMT1JPp53TIARtumor suppressor

Identifiers

PMID26909858
PMCPMC4941277
OpenAlexW2282578737

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.