Evidence map›Paper›PMID 27088889›Full record

ArticleCancer science2016

B7-H4 facilitates proliferation of esophageal squamous cell carcinoma cells through promoting interleukin-6/signal transducer and activator of transcription 3 pathway activation.

Xinran Chen, Ling Wang, Wei Wang, Lianmei Zhao, Baoen Shan

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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  10. An Immune-Related Gene Signature for Predicting Survival and Immunotherapy Efficacy in Esophageal Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Article
  11. Article
  12. Review
  13. Phenotypic and Functional Analyses of B7S1 in Ovarian Cancer.Frontiers in molecular biosciences · 2021
    Article
  14. Review
  15. 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

5 authors at 2 institutions in 1 country.

Xinran ChenResearch Center, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Ling WangHebei Cancer Research Institute, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Wei WangResearch Center, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Lianmei ZhaoResearch Center, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Baoen ShanResearch Center, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Fourth Hospital of Hebei Medical University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B7-H4, one of the costimulatory molecules of the B7 family, has been found to be widely expressed in many kinds of tumor tissues and to play an important part in tumor progression and poor prognosis. However, the role of B7-H4 in esophageal squamous cell carcinoma (ESCC) cells has not been elucidated. In this study, we found that, compared with normal esophageal tissue, B7-H4 was highly expressed in three ESCC cell lines, Eca109, TE1, and TE13. B7-H4 silenced cells suppressed cellular proliferation and colony formation. Additionally, compared with control cells, B7-H4 silenced cells showed higher apoptosis rates, Bcl-2 and Survivin upregulation, and BAX downregulation. Further study revealed that B7-H4 silenced cells also showed reduction in interleukin-6 (IL-6) secretion, signal transducer and activator of transcription 3 (STAT3) activation, and p-STAT3 translocation from cytoplasm to nucleus. Moreover, B7-H4 depletion inhibited the IL-6 secretion of control cells but not JAK2/STAT3 inhibitor FLLL32-treated cells. Interleukin-6 receptor antagonist tocilizumab did not block the p-JAK2 or p-STAT3 downregulation induced by B7-H4 silence. It was suggested that B7-H4 silence suppressed IL-6 secretion through JAK2/STAT3 inactivation. Furthermore, cell proliferation and colony formation were downregulated by tocilizumab in control cells but not in B7-H4 silenced cells, indicating that IL-6 upregulation induced by B7-H4 was necessary for cell growth. On the other hand, B7-H4 expression was downregulated by tocilizumab. In all, our study provided the first evidence that B7-H4 facilitated ESCC cell proliferation through promoting IL-6/STAT3 positive loopback pathway activation.

Indexed as

Signal TransductionAnimalsAntibodies, Monoclonal, HumanizedApoptosisCarcinoma, Squamous CellCell ProliferationCell Transformation, NeoplasticEsophageal NeoplasmsHumansInterleukin-6Janus Kinase 2MaleMiceMice, Inbred BALB CSTAT3 Transcription FactorTumor BurdenAntibodies, Monoclonal, HumanizedInterleukin-6Janus Kinase 2STAT3 protein, humanSTAT3 Transcription FactortocilizumabV-Set Domain-Containing T-Cell Activation Inhibitor 1VTCN1 protein, humanApoptosisB7-H4cell proliferationesophageal squamous cell carcinomaIL-6/STAT3 signal pathway

Identifiers

PMID27088889
PMCPMC4946714
OpenAlexW2483666230

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.