Evidence map›Paper›PMID 37037815›Full record

ArticleCell death discovery2023

Blocking the CXCL1-CXCR2 axis enhances the effects of doxorubicin in HCC by remodelling the tumour microenvironment via the NF-κB/IL-1β/CXCL1 signalling pathway.

Huiyong Zhao, Sheng Wei, Dachen Zhou, Yongfan Liu, Zicheng Guo, Chuibao Fang, Xiaoxi Pang, Fei Li, Hui Hou, Xiao Cui

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 22 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

10 authors at 1 institution in 1 country.

Huiyong Zhao *Department of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.ORCID http://orcid.org/0000-0003-0258-6327
Sheng Wei *Department of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Dachen ZhouDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Yongfan LiuDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Zicheng GuoDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Chuibao FangDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Xiaoxi PangDepartment of Nuclear Medicine, The Second Hospital of Anhui Medical University, Hefei, China.
Fei LiDepartment of Nuclear Medicine, The Second Hospital of Anhui Medical University, Hefei, China.
Hui HouDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China. Hui0402@hotmail.com.
Xiao CuiDepartment of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China. cx_2077@bjmu.edu.cn.ORCID http://orcid.org/0000-0003-0409-6073
Anhui Medical University · CN

Funding

Natural Science Foundation of Anhui Province (Anhui Provincial Natural Science Foundation) KJ2017A825
6 · The paper itself

Abstract

Inflammation is a core mechanism for oncogenesis. Chemokines act as important mediators of chronic inflammation and the tumour inflammatory response. However, there is limited information on chemokines in hepatocellular carcinoma (HCC), a disease for which almost all cases are derived from chronic liver inflammation. Here, we explored the protumor effects of CXCL1, a commonly elevated inflammatory chemokine in cirrhosis, in HCC. The protumor role was confirmed in clinical samples from HCC patients. CXCL1 enhanced tumorigenesis in the hepatic inflammatory microenvironment directly by acting on tumour cells and indirectly through promoting the recruitment of macrophages. The increase in the number of macrophages in the tumour microenvironment (TME) promoted tumour cell epithelial-mesenchymal transition (EMT) and significantly increased CXCL1 levels in the TME partly through NF-κB/IL-1β activation. To investigate the potential therapeutic value of CXCL1 in HCC with an inflammatory background, an antibody blocking CXCL1 was used alone or combined with the chemotherapy agent doxorubicin (DOX), with the goal of reshaping the TME. It has been shown that blocking CXCL1-CXCR2 inhibits tumour progression and reduces macrophage recruitment in the TME. The combination regimen has been shown to synergistically reduce the number of pro-tumour macrophages in the TME and suppress tumour progression. This provides insight into therapeutic strategies for treating HCC patients with high CXCL1 expression.

Identifiers

PMID37037815
PMCPMC10085981
OpenAlexW4363674696

What OpenQuestion holds

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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.