Evidence map›Paper›PMID 27602766›Full record

ArticleOncotarget2016

Rig-G is a growth inhibitory factor of lung cancer cells that suppresses STAT3 and NF-κB.

Dong Li, Junjun Sun, Wenfang Liu, Xuan Wang, Robert Bals, Junlu Wu, Wenqiang Quan, Yiwen Yao, Yu Zhang, Hong Zhou 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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Novel evidence for retinoic acid-induced G (Rig-G) as a tumor suppressor by activating p53 signaling pathway in lung cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  8. Review
  9. Article
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 2 countries.

Dong LiDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Junjun SunDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Wenfang LiuDepartment of General Surgery, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Xuan WangDepartment of Pharmacy, Putuo People's Hospital, 200060 Shanghai, China.
Robert BalsDepartment of Internal Medicine V - Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, 66424 Homburg, Germany.
Junlu WuDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Wenqiang QuanDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Yiwen YaoDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Yu ZhangDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Hong ZhouDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, 200065 Shanghai, China.
Kaiyin WuInstitute of Pathology, Charité Medical University, 10117 Berlin, Germany.
Tongji University · CNTongji Hospital · CNCentral Hospital of Putuo District · CNCharité - Universitätsmedizin Berlin · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of the retinoic acid-induced G (Rig-G) gene, an all trans retinoic acid (ATRA)-inducible gene, was observed in multiple cancer cells, including lung cancer cells. However, whether Rig-G is a tumor suppressor in lung cancer is unknown. Here, we found that ectopic expression of Rig-G can lead to a significant decrease in proliferation of lung cancer cells, resulting in an inhibition of tumor growth. Rig-G knockdown results in a modest increase in cell proliferation, as well as confers an increase in colony formation. Furthermore, transcriptome and pathway analyses of cancer cells revealed a fundamental impact of Rig-G on various growth signaling pathways, including the NF-κB pathway. Rig-G inhibits NF-κB activity by suppressing STAT3 in lung cancer cells. The downregulation of miR21 and miR181b-1 and subsequent activation of PTEN/Akt and CYLD/IκB signaling axis leading to decreased NF-κB activity required to maintain the tumor-inhibiting effect of Rig-G.. Our findings contribute to a better understanding of the antitumor effect mechanism of Rig-G, as well as offer a novel strategy for lung cancer therapy.

Indexed as

AnimalsApoptosisBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell ProliferationDeubiquitinating Enzyme CYLDDown-RegulationFemaleHumansI-kappa B ProteinsIntracellular Signaling Peptides and ProteinsLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMicroRNAsBiomarkers, TumorCYLD protein, humanDeubiquitinating Enzyme CYLDIFIT3 protein, humanI-kappa B ProteinsIntracellular Signaling Peptides and ProteinsMicroRNAsMIrn181 microRNA, humanMIRN21 microRNA, humanNF-kappa BProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanSTAT3 protein, humanSTAT3 Transcription Factorgrowth inhibitionlung cancerNF-κBRig-GSTAT3

Identifiers

PMID27602766
PMCPMC5323212
OpenAlexW2513256720

What OpenQuestion holds

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LicenceCC BY
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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.