Evidence map›Paper›PMID 37188659›Full record

ArticleOncogenesis2023

Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis.

Yujiu Gao, Yue Yuan, Shu Wen, Yanghui Chen, Zongli Zhang, Ying Feng, Bin Jiang, Shinan Ma, Rong Hu, Chen Fang and 7 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

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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

17 authors at 2 institutions in 1 country.

Yujiu Gao *Department of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Yue Yuan *Department of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Shu WenDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Yanghui ChenDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Zongli ZhangInstitute of Pediatric Disease, Taihe Hospital, 442000, Shiyan, China.
Ying FengDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Bin JiangDepartment of Hepatobiliary Pancreatic Surgery, Taihe Hospital, 442000, Shiyan, China.
Shinan MaDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Rong HuDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Chen FangDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Xuzhi RuanDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Yahong YuanDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Xinggang FangDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Chao LuoDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China.
Zhongji MengDepartment of Infectious Diseases, Institute of Biomedical Research, Hubei Clinical Research Center for Precise Diagnosis and Treatment of Liver Cancer, Taihe Hospital, 442000, Shiyan, China. zhongji.meng@163.com.ORCID http://orcid.org/0000-0003-0401-535X
Xiaoli WangDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China. xiaolitina@126.com.
Xingrong GuoDepartment of Critical Care Medicine, Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, China. gxrdl@126.com.
Hubei University of Medicine · CNTaihe Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82073232, 82101632, 81700769, 81641028
6 · The paper itself

Abstract

The interplay between hepatocellular carcinoma (HCC) cells and the tumor microenvironment is essential for hepatocarcinogenesis, but their contributions to HCC development are incompletely understood. We assessed the role of ANGPTL8, a protein secreted by HCC cells, in hepatocarcinogenesis and the mechanisms through which ANGPTL8 mediates crosstalk between HCC cells and tumor-associated macrophages. Immunohistochemical, Western blotting, RNA-Seq, and flow cytometry analyses of ANGPTL8 were performed. A series of in vitro and in vivo experiments were conducted to reveal the role of ANGPTL8 in the progression of HCC. ANGPTL8 expression was positively correlated with tumor malignancy in HCC, and high ANGPTL8 expression was associated with poor overall survival (OS) and disease-free survival (DFS). ANGPTL8 promoted HCC cell proliferation in vitro and in vivo, and ANGPTL8 KO inhibited the development of HCC in both DEN-induced and DEN-plus-CCL4-induced mouse HCC tumors. Mechanistically, the ANGPTL8-LILRB2/PIRB interaction promoted polarization of macrophages to the immunosuppressive M2 phenotype in macrophages and recruited immunosuppressive T cells. In hepatocytes, ANGPTL8-mediated stimulation of LILRB2/PIRB regulated the ROS/ERK pathway and upregulated autophagy, leading to the proliferation of HCC cells. Our data support the notion that ANGPTL8 has a dual role in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis.

Identifiers

PMID37188659
PMCPMC10185523
OpenAlexW4376641028

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.