Evidence map›Paper›PMID 28152516›Full record

ArticleOncotarget2017

TNFAIP8 interacts with LATS1 and promotes aggressiveness through regulation of Hippo pathway in hepatocellular carcinoma.

Qianze Dong, Lin Fu, Yue Zhao, Chengyao Xie, Qingchang Li, Enhua Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. TNFAIP8 drives metabolic reprogramming to promote prostate cancer cell proliferation.The international journal of biochemistry & cell biology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. TNFAIP8: Inflammation, Immunity and Human Diseases.Journal of cellular immunology · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. TIPE Family of Proteins and Its Implications in Different Chronic Diseases.International journal of molecular sciences · 2018
    Review
  17. Article
  18. Article
  19. Review
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

6 authors at 1 institution in 1 country.

Qianze DongCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
Lin FuCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
Yue ZhaoCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
Chengyao XieCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
Qingchang LiCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
Enhua WangCollege of Basic Medical Sciences and Department of Pathology, First Affiliated Hospital, China Medical University Shenyang, Liaoning, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although TNFAIP8 overexpression has been implicated in several human cancers, its clinical significance and biological function in hepatocellular carcinoma (HCC) remains unknown. Our study demonstrated that TNFAIP8 overexpression in primary HCC samples correlated with TNM stage, recurrence, poor prognosis and served as an independent favorable prognostic factor. We further showed that TNFAIP8 upregulated cell proliferation, migration, invasion and xenograft tumor growth of HCC cells. In addition, TNFAIP8 overexpression inhibited YAP phosphorylation, increased its nuclear localization and stabilization, leading to upregulation of cyclin proteins, CTGF and cell proliferation. We also found that TNFAIP8 could interact with LATS1 and decreased its phosphorylation. Depletion of LATS1 and YAP by siRNA blocked the biological effects of TNFAIP8. Collectively, the present study provides a novel finding that TNFAIP8 promotes HCC progression through LATS1-YAP signaling pathway. TNFAIP8 may serve as a candidate biomarker for poor prognosis and a target for new therapies.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBlotting, WesternCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHep G2 CellsHippo KinasesHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsKaplan-Meier EstimateAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsHippo KinasesIntracellular Signaling Peptides and ProteinsLATS1 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesSerine-Threonine Kinase 3STK3 protein, humanSTK4 protein, humanTNFAIP8 protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling Proteinshepatocellular carcinomaHippoTNFAIP8YAP

Identifiers

PMID28152516
PMCPMC5362516
OpenAlexW2583345756

What OpenQuestion holds

Textmetadata
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.