Evidence map›Paper›PMID 24332041›Full record

ArticleCancer cell2013

NCOA5 haploinsufficiency results in glucose intolerance and subsequent hepatocellular carcinoma.

Shenglan Gao, Aimin Li, Feiye Liu, Fengsheng Chen, Mark Williams, Chengliang Zhang, Zakiya Kelley, Chin-Lee Wu, Rongcheng Luo, Hua Xiao

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

Article in Cancer cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  8. NCOA5 Deficiency in Macrophages Provokes NASH and HCC.Cellular and molecular gastroenterology and hepatology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Shenglan GaoDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA; Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA.
Aimin LiDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA; Cancer Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Feiye LiuCancer Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Fengsheng ChenDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA; Cancer Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Mark WilliamsDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA; Cell and Molecular Biology Program, Michigan State University, East Lansing, MI 48824, USA.
Chengliang ZhangDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Zakiya KelleyDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA.
Chin-Lee WuDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Rongcheng LuoCancer Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: luorc01@163.com.
Hua XiaoDepartment of Physiology, Michigan State University, East Lansing, MI 48824, USA. Electronic address: xiaoh@msu.edu.
Michigan State University · USNanfang Hospital · CNMassachusetts General Hospital · USSouthern Medical University · CN

Funding

Integrative Training in the Pharmacological SciencesT32GM092715 · NIGMS · MICHIGAN STATE UNIVERSITY · PI NEUBIG, RICHARD R · 2011 to 2020
$1.5M
NcoA5, a unique nuclear receptor coactivator in hepatocarcinogenesisR21CA158539 · NCI · MICHIGAN STATE UNIVERSITY · PI XIAO, HUA · 2011 to 2012
$347k
NCI NIH HHS 1R21CA158539NCI NIH HHS R21 CA158539NIGMS NIH HHS T32 GM092715
6 · The paper itself

Abstract

Type 2 diabetes (T2D) and male gender are associated with hepatocellular carcinoma (HCC) development. We demonstrate that heterozygous deletion of the Ncoa5 gene causes spontaneous development of HCC exclusively in male mice. Tumor development is preceded by increased interleukin-6 (IL-6) expression, early-onset glucose intolerance, and progressive steatosis and dysplasia in livers. Blockading IL-6 overexpression averts glucose intolerance and partially deters HCC development. Moreover, reduced NCOA5 expression is associated with a fraction of human HCCs and HCCs with comorbid T2D. These findings suggest that NCOA5 is a haploinsufficient tumor suppressor and that NCOA5 deficiency increases susceptibility to both glucose intolerance and HCC, partially by increasing IL-6 expression. Thus, our findings open additional avenues for developing therapeutic approaches to combat these diseases.

Indexed as

HaploinsufficiencyAdultAgedAnimalsCarcinoma, HepatocellularFatty LiverFemaleGlucose IntoleranceHumansInterleukin-6Liver NeoplasmsMaleMiceMice, Inbred BALB CMice, Inbred C57BLMiddle AgedInterleukin-6NCOA5 protein, humanNuclear Receptor CoactivatorsReceptors, AndrogenSTAT3 Transcription Factor

Identifiers

PMID24332041
PMCPMC3891053
OpenAlexW2003379778

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.