Evidence map›Paper›PMID 27050273›Full record

ArticleOncotarget2016

Apoptosis signal-regulating kinase 1 mediates the inhibitory effect of hepatocyte nuclear factor-4α on hepatocellular carcinoma.

Cai-Feng Jiang, Liang-Zhi Wen, Chuan Yin, Wen-Ping Xu, Bin Shi, Xin Zhang, Wei-Fen Xie

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Hepatocyte Nuclear Factor 4 Alpha: A Key Regulator of Liver Disease Pathology and Haemostatic Disorders.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Review
  3. SDS3 regulates microglial inflammation by modulating the expression of the upstream kinase ASK1 in the p38 MAPK signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  4. Review
  5. Review
  6. Review
  7. ASK1 inhibition: a therapeutic strategy with multi-system benefits.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  8. Article
  9. Review
  10. 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

7 authors at 1 institution in 1 country.

Cai-Feng JiangDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Liang-Zhi WenDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Chuan YinDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Wen-Ping XuDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Bin ShiDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Xin ZhangDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Wei-Fen XieDepartment of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies provided substantial evidence of a striking suppressive effect of hepatocyte nuclear factor 4α (HNF4α) on hepatocellular carcinoma (HCC). Apoptosis signal-regulating kinase 1 (ASK1) is involved in death receptor-mediated apoptosis and may acts as a tumor suppressor in hepatocarcinogenesis. However, the status and function of ASK1 during HCC progression are unclear. In this study, we found that HNF4α increased ASK1 expression by directly binding to its promoter. ASK1 expression was dramatically suppressed and correlated with HNF4α levels in HCC tissues. Reduced ASK1 expression was associated with aggressive tumors and poor prognosis for human HCC. Moreover, ASK1 inhibited the malignant phenotype of HCC cells in vitro. Intratumoral ASK1 injection significantly suppressed the growth of subcutaneous HCC xenografts in nude mice. More interestingly, systemic ASK1 delivery strikingly inhibited the growth of orthotopic HCC nodules in NOD/SCID mice. In addition, inhibition of endogenous ASK1 partially reversed the suppressive effects of HNF4α on HCC. Collectively, this study highlights the suppressive effect of ASK1 on HCC and its biological significance in HCC development. These outcomes broaden the knowledge of ASK1 function in HCC progression, and provide a novel potential prognostic biomarker and therapeutic target for advanced HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorGene Expression ProfilingGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 4HumansLiver NeoplasmsMaleMAP Kinase Kinase Kinase 5MAP Kinase Signaling SystemMice, Inbred BALB CMice, Inbred NODMice, NudeMice, SCIDPromoter Regions, GeneticHepatocyte Nuclear Factor 4HNF4A protein, humanMAP3K5 protein, humanMAP Kinase Kinase Kinase 5apoptosis signal-regulating kinase 1differentiation therapyhepatocellular carcinomahepatocyte nuclear factor 4αmitogen-activated protein kinases

Identifiers

PMID27050273
PMCPMC5053659
OpenAlexW2322088624

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.