Evidence map›Paper›PMID 32831137›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

LINC00669 insulates the JAK/STAT suppressor SOCS1 to promote nasopharyngeal cancer cell proliferation and invasion.

Xiang Qing, Guo-Lin Tan, Huo-Wang Liu, Wei Li, Jin-Gang Ai, Shan-Shan Xiong, Meng-Qing Yang, Tian-Sheng Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  20. Ferroptosis DriverFrontiers in cell and developmental biology · 2021
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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

8 authors at 2 institutions in 1 country.

Xiang QingDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Guo-Lin TanDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Huo-Wang LiuDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Wei LiDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Jin-Gang AiDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Shan-Shan XiongDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Meng-Qing YangDepartment of Postgraduate Office, Third Xiangya Hospital, Central South University, Changsha, 410013, China.
Tian-Sheng WangDepartment of Otolaryngology Head and Neck Surgery, The Third Xiangya Hospital, Central South University, Changsha, 410013, China. tianshengwang@csu.edu.cn.
Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is an epithelial cancer emerging from the lining of nasopharyngeal mucosa, with extremely frequent occurrence in east and southeast Asia. For the purpose of exploring roles of the dysregulated long non-coding RNA (lncRNA) in NPC, we identified a novel lncRNA LINC00669 with an apparent negative correlation to the overall survival from human NPC mRNA expression profiling databases. We further performed RNA pulldown coupled with mass spectrum to find out its target protein, and applied a series of in vitro and in vivo loss-and-gain-of function assays to investigate its oncogenic roles in NPC tumor development and progression. Our results demonstrated that LINC00669 competitively binds to the key JAK/STAT signaling pathway suppressor SOCS1, and insulates it from imposing ubiquitination modification on the pathway component of STAT1, which leads to its abnormal stabilization and activation. The activated STAT1 is then transferred into the nucleus and initiates the transcription of genes related to proliferation and invasion. In summary, our study reveals that the cytoplasmic resident lncRNA LINC00669 confers malignant properties on NPC cancer cells by facilitating a persistent activation of the JAK/STAT signaling pathway. Findings in the current study shed lights on prospects for treating NPC using strategies targeting the novel regulator of the JAK/STAT signaling.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationHumansJanus Kinase 1MaleMiceMice, Inbred BALB CMice, NudeNasopharyngeal NeoplasmsNeoplasm InvasivenessPrognosisRNA, Long NoncodingBiomarkers, TumorJAK1 protein, humanJanus Kinase 1RNA, Long NoncodingSOCS1 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinJAK/STATLINC00669Long non-coding RNANasopharyngeal carcinomaSOCS1STAT1

Identifiers

PMID32831137
PMCPMC7444085
OpenAlexW3080912413

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Registered trials

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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.