Evidence map›Paper›PMID 27273788›Full record

ArticleInternational journal of cancer2016

Dysregulated hepatic bile acids collaboratively promote liver carcinogenesis.

Guoxiang Xie, Xiaoning Wang, Fengjie Huang, Aihua Zhao, Wenlian Chen, Jingyu Yan, Yunjing Zhang, Sha Lei, Kun Ge, Xiaojiao Zheng and 4 more

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

148 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.

  1. The Human Microbiome in Relation to Cancer Risk: A Systematic Review of Epidemiologic Studies.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Pooled it
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  12. The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026
    Review
  13. mSystems · 2026
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88 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 2 countries.

Guoxiang XieShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Xiaoning WangE-Institute of Shanghai Municipal Education Committee, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Fengjie HuangShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Aihua ZhaoShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Wenlian ChenMetabolomics Shared Resource, University of Hawaii Cancer Center, Honolulu, HI.
Jingyu YanE-Institute of Shanghai Municipal Education Committee, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yunjing ZhangShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Sha LeiShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Kun GeShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Xiaojiao ZhengShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Jiajian LiuShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Mingming SuMetabolomics Shared Resource, University of Hawaii Cancer Center, Honolulu, HI.
Ping LiuE-Institute of Shanghai Municipal Education Committee, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Wei JiaShanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CNShanghai Municipal Education Commission · CNCancer Center of Hawaii · USShuguang Hospital · CNUniversity of Hawaiʻi at Mānoa · US

Funding

University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI Xin Chen · 1996 to 2026
$56.2M
Gut microbiota mediated bile acid alterations in hepatic carcinogenesisU01CA188387 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI JIA, WEI · 2015 to 2019
$2.7M
NCI NIH HHS P30 CA071789NCI NIH HHS U01 CA188387
6 · The paper itself

Abstract

Dysregulated bile acids (BAs) are closely associated with liver diseases and attributed to altered gut microbiota. Here, we show that the intrahepatic retention of hydrophobic BAs including deoxycholate (DCA), taurocholate (TCA), taurochenodeoxycholate (TCDCA), and taurolithocholate (TLCA) were substantially increased in a streptozotocin and high fat diet (HFD) induced nonalcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC) mouse model. Additionally chronic HFD-fed mice spontaneously developed liver tumors with significantly increased hepatic BA levels. Enhancing intestinal excretion of hydrophobic BAs in the NASH-HCC model mice by a 2% cholestyramine feeding significantly prevented HCC development. The gut microbiota alterations were closely correlated with altered BA levels in liver and feces. HFD-induced inflammation inhibited key BA transporters, resulting in sustained increases in intrahepatic BA concentrations. Our study also showed a significantly increased cell proliferation in BA treated normal human hepatic cell lines and a down-regulated expression of tumor suppressor gene CEBPα in TCDCA treated HepG2 cell line, suggesting that several hydrophobic BAs may collaboratively promote liver carcinogenesis.

Indexed as

AnimalsBile Acids and SaltsCarcinogenesisCell LineDeoxycholic AcidDiet, High-FatFemaleGastrointestinal MicrobiomeHep G2 CellsHumansLiver NeoplasmsLiver Neoplasms, ExperimentalMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseBile Acids and SaltsDeoxycholic AcidStreptozocinTaurochenodeoxycholic AcidTaurocholic AcidTaurolithocholic Acidbile acidsgut microbiotainflammationliver carcinogenesisproliferation

Identifiers

PMID27273788
PMCPMC5493524
OpenAlexW2409636417

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.