Evidence map›Paper›PMID 35294987›Full record

ArticleCancer science2022

Histone H1.2 promotes hepatocarcinogenesis by regulating signal transducer and activator of transcription 3 signaling.

Qing Wang, Yuchen Chen, Yunhao Xie, Dong Yang, Yuyan Sun, Yangmian Yuan, Hong Chen, Yu Zhang, Kun Huang, Ling Zheng

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Histone Demethylase UTX Suppresses Tumor Cell Proliferation by Regulating Stress Granules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

10 authors at 2 institutions in 1 country.

Qing WangHubei Key Laboratory of Cell Homeostasis, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, China.
Yuchen ChenTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yunhao XieHubei Key Laboratory of Cell Homeostasis, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, China.
Dong YangTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yuyan SunHubei Key Laboratory of Cell Homeostasis, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, China.
Yangmian YuanHubei Key Laboratory of Cell Homeostasis, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, China.
Hong ChenTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yu ZhangTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Kun HuangTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID https://orcid.org/0000-0002-0808-2325
Ling ZhengHubei Key Laboratory of Cell Homeostasis, Frontier Science Center for Immunology and Metabolism, College of Life Sciences, Wuhan University, Wuhan, China.
Huazhong University of Science and Technology · CNWuhan University · CN

Funding

National Key R&D Program of China 2018YFA0800700National Key R&D Program of China 2019YFA0802701Natural Science Foundation of China 31871381Natural Science Foundation of China 32021003Natural Science Foundation of China 91957114Natural Science Foundation of Hubei Province 2021CFA004
6 · The paper itself

Abstract

Linker histone H1.2 (H1.2), encoded by HIST1H1C (H1C), is a major H1 variant in somatic cells. Among five histone H1 somatic variants, upregulated H1.2 was found in human hepatocellular carcinoma (HCC) samples and in a diethylnitrosamine (DEN)-induced HCC mouse model. In vitro, H1.2 overexpression accelerated proliferation of HCC cell lines, whereas H1.2 knockdown (KD) had the opposite effect. In vivo, H1.2 insufficiency or deficiency (H1c KD or H1c KO) alleviated inflammatory response and HCC development in DEN-treated mice. Mechanistically, H1.2 regulated the activation of signal transducer and activator of transcription 3 (STAT3), which in turn positively regulated H1.2 expression by binding to its promoter. Moreover, upregulation of the H1.2/STAT3 axis was observed in human HCC samples, and was confirmed in mouse models of methionine-choline-deficient diet induced nonalcoholic steatohepatitis or lipopolysaccharide induced acute inflammatory liver injury. Disrupting this feed-forward loop by KD of STAT3 or treatment with STAT3 inhibitors rescued H1.2 overexpression-induced proliferation. Moreover, STAT3 inhibitor treatment-ameliorated H1.2 overexpression promoted xenograft tumor growth. Therefore, H1.2 plays a novel role in inflammatory response by regulating STAT3 activation in HCC, thus, blockade of the H1.2/STAT3 loop is a potential strategy against HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsCarcinogenesisCell Line, TumorCell ProliferationDisease Models, AnimalHistonesHumansMiceSignal TransductionSTAT3 Transcription FactorHistonesSTAT3 Transcription Factorfeed-forward loophepatocellular carcinomahistone H1.2inflammationSTAT3

Identifiers

PMID35294987
PMCPMC9128180
OpenAlexW4220828018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.