Evidence map›Paper›PMID 31375423›Full record

ArticleEBioMedicine2019

Hepatectomy promotes recurrence of liver cancer by enhancing IL-11-STAT3 signaling.

Dongyao Wang, Xiaohu Zheng, Binqing Fu, Zhigang Nian, Yeben Qian, Rui Sun, Zhigang Tian, Haiming Wei

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Article
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  4. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
    Review
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  18. Alcohol reshapes a liver premetastatic niche for cancer by extra- and intrahepatic crosstalk-mediated immune evasion.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Dongyao WangDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiaohu ZhengDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
Binqing FuDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
Zhigang NianDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
Yeben QianDepartment of General Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230027, China.
Rui SunDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China.
Zhigang TianDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: tzg@ustc.edu.cn.
Haiming WeiDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China; Institute of Immunology, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: ustcwhm@ustc.edu.cn.
University of Science and Technology of China · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients undergoing surgical resection of hepatocellular carcinoma (HCC) are at risk of recurrence; however, the underlying mechanism remains poorly understood.

methodsThrough the analysis of gene expression profiles in tumour and matched normal tissues from patients with hepatocellular carcinoma (HCC), we identified differences in interleukin-11 (IL-11) expression. Further, we used genetic mouse, orthotopic tumour, chemically induced, and orthotopic allograft models to study the correlation between IL-11 and postsurgical recurrence. Additionally, we conducted a series of experiments, including histology and immunohistochemistry analysis, three-dimensional culture, immunofluorescence, western blotting, enzyme-linked immunosorbent assay (ELISA) and flow cytometry to investigate the role of IL-11-signal transducer and activator of transcription 3 (STAT3) signaling in HCC recurrence.

findingsWe demonstrate that IL-11 levels increase after surgery, triggering HCC outgrowth. Accordingly, pharmacological blocking of IL-11-STAT3 signaling in model systems significantly alleviates tumour cell proliferation and suppresses postsurgical recurrence of HCC tumours.

interpretationThese data demonstrate that IL-11 has a central role in postsurgical HCC recurrence, and that inhibition of IL-11-STAT3 signaling is a potential therapeutic strategy to prevent recurrence. FUND: Natural Science Foundation of China.

Indexed as

Signal TransductionAnimalsApoptosisBiomarkersCell Line, TumorDisease Models, AnimalGene ExpressionHepatectomyHeterograftsHumansImmunohistochemistryInterleukin-11Liver NeoplasmsMaleMiceMice, KnockoutBiomarkersInterleukin-11STAT3 Transcription FactorHepatocellular carcinomaIL-11-STAT3 signalingNapabucasinRecurrenceSurgical resection

Identifiers

PMID31375423
PMCPMC6711863
OpenAlexW2965119488

What OpenQuestion holds

Textmetadata
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.