Evidence map›Paper›PMID 29540666›Full record

ArticleCell death & disease2018

Histone deacetylase 3 promotes liver regeneration and liver cancer cells proliferation through signal transducer and activator of transcription 3 signaling pathway.

Xu-Feng Lu, Xiao-Yue Cao, Yong-Jie Zhu, Zhen-Ru Wu, Xiang Zhuang, Ming-Yang Shao, Qing Xu, Yong-Jie Zhou, Hong-Jie Ji, Qing-Richard Lu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

38 citing papers in PubMed, 148 citations in OpenAlex.

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  11. GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024
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  12. Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024
    Review
  13. Review
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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

13 authors at 4 institutions in 2 countries.

Xu-Feng LuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Xiao-Yue CaoLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Yong-Jie ZhuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhen-Ru WuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Xiang ZhuangLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Ming-Yang ShaoLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Qing XuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Yong-Jie ZhouLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Hong-Jie JiLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
Qing-Richard LuDepartment of Pediatrics, Division of Experimental Hematology and Cancer Biology, Brain Tumor Center, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 25229, USA.
Yu-Jun ShiLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China. shiyujun@scu.edu.cn.
Yong ZengDepartment of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, 610041, China.
Hong BuLaboratory of Pathology, Key Laboratory of Transplant Engineering and Immunology, NHFPC; West China Hospital, Sichuan University, Chengdu, 610041, China.
National Health and Family Planning Commission · CNWest China Hospital of Sichuan University · CNSichuan University · CNCincinnati Children's Hospital Medical Center · US

Funding

Molecular Mechanisms of Oligodendrocyte Differentiation and MyelinationR01NS072427 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2010 to 2018
$3.6M
Chromatin remodeling control of myelination and remyelinationR01NS075243 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2018
$2.6M
Molecular and signaling mechanisms of peripheral nerve sheath tumorigenesisR37NS096359 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI LU, QING R · 2016 to 2018
$1.6M
NINDS NIH HHS R01 NS072427NINDS NIH HHS R01 NS075243NINDS NIH HHS R37 NS096359
6 · The paper itself

Abstract

Histone deacetylase 3 (HDAC3) plays pivotal roles in cell cycle regulation and is often aberrantly expressed in various cancers including hepatocellular carcinoma (HCC), but little is known about its role in liver regeneration and liver cancer cells proliferation. Using an inducible hepatocyte-selective HDAC3 knockout mouse, we find that lack of HDAC3 dramatically impaired liver regeneration and blocked hepatocyte proliferation in the G1 phase entry. HDAC3 inactivation robustly disrupted the signal transducer and activator of transcription 3 (STAT3) cascade. HDAC3 silencing impaired the ac-STAT3-to-p-STAT3 transition in the cytoplasm, leading to the subsequent breakdown of STAT3 signaling. Furthermore, overexpressed HDAC3 was further associated with increased tumor growth and a poor prognosis in HCC patients. Inhibition of HDAC3 expression reduced liver cancer cells growth and inhibited xenograft tumor growth. Our results suggest that HDAC3 is an important regulator of STAT3-dependent cell proliferation in liver regeneration and cancer. These findings provide novel insights into the HDAC3-STAT3 pathway in liver pathophysiological processes.

Indexed as

AnimalsCell ProliferationHepatocytesHistone Deacetylase 3Histone DeacetylasesHumansLiver NeoplasmsLiver RegenerationMaleMiceMice, KnockoutSignal TransductionSTAT3 Transcription FactorHistone Deacetylase 3Histone DeacetylasesSTAT3 Transcription Factor

Identifiers

PMID29540666
PMCPMC5852132
OpenAlexW2794396622

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.