Evidence map›Paper›PMID 38724465›Full record

ArticleJournal for immunotherapy of cancer2024

CD276 regulates the immune escape of esophageal squamous cell carcinoma through CXCL1-CXCR2 induced NETs.

Gan Xiong, Zhi Chen, Qianwen Liu, Fang Peng, Caihua Zhang, Maosheng Cheng, Rongsong Ling, Shuang Chen, Yu Liang, Demeng Chen and 1 more

Abstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. VPS9D1-AS1: a critical oncogenic long non-coding RNA in human malignancies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  13. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    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

11 authors.

Gan Xiong *Center for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Zhi Chen *Center for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Qianwen Liu *Department of Thoracic Oncology, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Fang Peng *Department of Radiation Oncology, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Caihua Zhang *Center for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Maosheng ChengCenter for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Rongsong LingInstitute for Advanced Study, Shenzhen University, Shenzhen, Guangdong, China.
Shuang ChenCenter for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Yu LiangCenter for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China.
Demeng ChenCenter for Translational Medicine, Sun Yat-sen University First Affiliated Hospital, Guangzhou, Guangdong, China qimin.zhou@sjtu.edu.cn chendm29@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-7230-2495
Qimin ZhouDepartment of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China qimin.zhou@sjtu.edu.cn chendm29@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-9480-4872

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD276 (B7-H3), a pivotal immune checkpoint, facilitates tumorigenicity, invasiveness, and metastasis by escaping immune surveillance in a variety of tumors; however, the underlying mechanisms facilitating immune escape in esophageal squamous cell carcinoma (ESCC) remain enigmatic.

methodsWe investigated the expression of CD276 in ESCC tissues from patients by using immunohistochemistry (IHC) assays. In vivo, we established a 4-nitroquinoline 1-oxide (4NQO)-induced CD276 knockout (CD276

resultsIn this study, we elucidate that CD276 is markedly upregulated in ESCC, correlating with poor prognosis. In vivo, our results indicate that depletion of CD276 inhibits tumorigenesis and progression of ESCC. Furthermore, conditional knockout of CD276 in epithelial cells engenders a significant downregulation of CXCL1, consequently reducing the formation of neutrophil extracellular trap networks (NETs) via the CXCL1-CXCR2 signaling axis, while simultaneously augmenting natural killer (NK) cells. In addition, overexpression of CD276 promotes tumorigenesis via increasing NETs' formation and reducing NK cells in vivo.

conclusionsThis study successfully elucidates the functional role of CD276 in ESCC. Our comprehensive analysis uncovers the significant role of CD276 in modulating immune surveillance mechanisms in ESCC, thereby suggesting that targeting CD276 might serve as a potential therapeutic approach for ESCC treatment.

Indexed as

B7 AntigensEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaExtracellular TrapsAnimalsChemokine CXCL1FemaleHumansMaleMiceMice, KnockoutReceptors, Interleukin-8BTumor EscapeTumor MicroenvironmentB7 AntigensCD276 protein, humanChemokine CXCL1CXCR2 protein, humanReceptors, Interleukin-8BEsophageal CancerImmune Checkpoint InhibitorNatural killer - NK

Identifiers

PMID38724465
PMCPMC11086492

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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.