Evidence map›Paper›PMID 36898011›Full record

ArticleCancer immunology research2023

HDAC3 Inhibition Promotes Antitumor Immunity by Enhancing CXCL10-Mediated Chemotaxis and Recruiting of Immune Cells.

Lili Li, Shumin Hao, Meiling Gao, Junxiao Liu, Xin Xu, Jianfei Huang, Genhong Cheng, Heng Yang

Open access · hybridAbstract read
In one paragraph

Article in Cancer immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 44 citations in OpenAlex.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
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  20. Targeting HDAC and PARP Enhances STING-Dependent Antitumor Immunity in STING-Deficient Tumor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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

8 authors at 4 institutions in 2 countries.

Lili Li *Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0002-0895-244X
Shumin Hao *Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0002-0265-9218
Meiling Gao *Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0001-6893-5716
Junxiao Liu *Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0002-0187-7862
Xin XuInstitute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0003-4063-000X
Jianfei HuangDepartment of Clinical Biobank, Affiliated Hospital of Nantong University, Nantong, P.R. China.ORCID 0000-0002-1276-5962
Genhong ChengDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles.ORCID 0000-0002-6713-2783
Heng YangInstitute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P.R. China.ORCID 0000-0002-1491-4490
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNantong University · CNShanghai Medical College of Fudan University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is generally believed that histone deacetylase (HDAC) inhibitors, which represent a new class of anticancer agents, exert their antitumor activity by directly causing cell-cycle arrest and apoptosis of tumor cells. However, in this study, we demonstrated that class I HDAC inhibitors, such as Entinostat and Panobinostat, effectively suppressed tumor growth in immunocompetent but not immunodeficient mice. Further studies with Hdac1, 2, or 3 knockout tumor cells indicated that tumor-specific inactivation of HDAC3 suppressed tumor growth by activating antitumor immunity. Specifically, we found that HDAC3 could directly bind to promotor regions and inhibit the expression of CXCL9, 10, and 11 chemokines. Hdac3-deficient tumor cells expressed high levels of these chemokines, which suppressed tumor growth in immunocompetent mice by recruiting CXCR3+ T cells into the tumor microenvironment (TME). Furthermore, the inverse correlation between HDAC3 and CXCL10 expression in hepatocellular carcinoma tumor tissues also suggested HDAC3 might be involved in antitumor immune regulation and patient survival. Thus, our studies have illustrated that HDAC3 inhibition suppresses tumor growth by enhancing immune cell infiltration into the TME. This antitumor mechanism may be helpful in guiding HDAC3 inhibitor-based treatment.

Indexed as

Antineoplastic AgentsLiver NeoplasmsAnimalsCell Line, TumorChemokine CXCL10ChemotaxisHistone Deacetylase InhibitorsMiceTumor MicroenvironmentAntineoplastic AgentsChemokine CXCL10Cxcl10 protein, mouseHistone Deacetylase Inhibitors

Identifiers

PMID36898011
PMCPMC10155037
OpenAlexW4323825217

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.