Evidence map›Paper›PMID 29152756›Full record

ArticleHepatology (Baltimore, Md.)2018

β-catenin deficiency in hepatocytes aggravates hepatocarcinogenesis driven by oncogenic β-catenin and MET.

Yan Liang, Yun Feng, Min Zong, Xu-Fu Wei, Jin Lee, Yukuan Feng, Hairi Li, Guang-Shun Yang, Zhong-Jun Wu, Xiang-Dong Fu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Manipulating the EphB4-ephrinB2 axis to reduce metastasis in HNSCC.bioRxiv : the preprint server for biology · 2024
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Loss of CTNNB1 exon 3 in sclerosing angiomatoid nodular transformation of the spleen.Virchows Archiv : an international journal of pathology · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Development and Validation of a Novel Immune-Gene Pairs Prognostic Model Associated with CTNNB1 Alteration in Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  18. Article
  19. Review
  20. The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020
    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

11 authors at 4 institutions in 2 countries.

Yan LiangDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
Yun FengDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
Min ZongDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
Xu-Fu WeiDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
Jin LeeDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
Yukuan FengDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA.
Hairi LiDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA.
Guang-Shun YangFifth Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.
Zhong-Jun WuDepartment of Hepatology, First Affiliated Hospital, Chong-Qing Medical University, Chong-Qing, China.
Xiang-Dong FuDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA.
Gen-Sheng FengDepartment of Pathology and Division of Biological Sciences, Moores Cancer Center, University of California San Diego, La Jolla, CA.
University of California, San Diego · USSecond Military Medical University · CNEastern Hepatobiliary Surgery Hospital · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

Regulation of RNA metabolism and cell growth control by SR protein kinasesR01GM052872 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DOWDY, STEVEN F · 1996 to 2019
$5.4M
Dissection of Pten-regulated signals in hepatopathogenesisR01CA188506 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FENG, GEN-SHENG · 2015 to 2019
$1.9M
Molecular and Cellular Communications in Liver TumorigenesisR01CA176012 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FENG, GEN-SHENG · 2014 to 2019
$1.7M
NCI NIH HHS R01 CA176012NCI NIH HHS R01 CA188506NIGMS NIH HHS R01 GM052872
6 · The paper itself

Abstract

Both activating and inactivating mutations in catenin β1 (ctnnb1), which encodes β-catenin, have been implicated in liver tumorigenesis in humans and mice, although the underlying mechanisms are not fully understood. Herein, we show that deletion of endogenous β-catenin in hepatocytes aggravated hepatocellular carcinoma (HCC) development driven by an oncogenic version of β-catenin (CAT) in combination with the hepatocyte growth factor receptor MET proto-oncogene receptor tyrosine kinase (MET). Although the mitogenic signaling and cell cycle progression was modestly impaired after CAT/MET transfection, the β-catenin-deficient livers displayed changes in transcriptomes, increased DNA damage response, expanded Sox9

conclusionThese data argue that while dominantly activating mutants of β-catenin are oncogenic, inhibiting the oncogenic signaling pathway generates a pro-oncogenic microenvironment that may facilitate HCC recurrence following a targeted therapy of the primary tumor. An effective therapeutic strategy must require disruption of the oncogenic signaling in tumor cells and suppression of the secondary tumor-promoting stromal effects in the liver microenvironment. (Hepatology 2018;67:1807-1822).

Indexed as

Animalsbeta CateninCarcinogenesisCarcinoma, HepatocellularGene Expression ProfilingGene Expression Regulation, NeoplasticHepatocytesHumansLiverLiver NeoplasmsMiceOncogenesProto-Oncogene MasProto-Oncogene Proteins c-metSignal Transductionbeta CateninCTNNB1 protein, humanMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-met

Identifiers

PMID29152756
PMCPMC5906147
OpenAlexW2769590730

What OpenQuestion holds

Textmetadata
LicenceTDM
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.