Evidence map›Paper›PMID 38183060›Full record

ArticleCell communication and signaling : CCS2024

Hypoxia-induced ZEB1 promotes cervical cancer immune evasion by strengthening the CD47-SIRPα axis.

Xiao-Jing Chen, Chu-Hong Guo, Zi-Ci Wang, Yang Yang, Yu-Hua Pan, Jie-Ying Liang, Mei-Ge Sun, Liang-Sheng Fan, Li Liang, Wei Wang

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.7field-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

20 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Effect of Extracellular Vesicles Derived From Tumor Cells on Immune Evasion.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.

Xiao-Jing Chen *Guangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Chu-Hong Guo *Guangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Zi-Ci WangGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Yang YangGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Yu-Hua PanGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Jie-Ying LiangGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Mei-Ge SunGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China.
Liang-Sheng FanGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China. fanyi0606@163.com.
Li LiangDepartment of Pathology, Nanfang Hospital, Southern Medical University, 1838 Guangzhou Avenue North, Baiyun District, Guangzhou, 510515, People's Republic of China. lli@fimmu.com.
Wei WangGuangzhou Medical University/Department of Obstetrics and Gynecology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiang West Road, Yuexiu District, Guangzhou, 510120, People's Republic of China. 2017991016@gzhmu.edu.cn.
First Affiliated Hospital of Guangzhou Medical University · CNNanfang Hospital · CN

Funding

China Postdoctoral Science Foundation 2020M682674Guangdong Basic and Applied Basic Research Foundation-the Regional Joint Fund 2020A1515110924Guangzhou Science and Technology Program key Project 202102010223National Key R&D Program of China 2021YFC2701205National Natural Science Foundation of China 81971341National Natural Science Foundation of China 82101704Natural Science Foundation of Guangdong Province 2019A1515010872Natural Science Foundation of Guangdong Province 2022A1515010530
6 · The paper itself

Abstract

backgroundThe dynamic interaction between cancer cells and tumour-associated macrophages (TAMs) in the hypoxic tumour microenvironment (TME) is an active barrier to the effector arm of the antitumour immune response. Cancer-secreted exosomes are emerging mediators of this cancer-stromal cross-talk in the TME; however, the mechanisms underlying this interaction remain unclear.

methodsExosomes were isolated with ExoQuick exosome precipitation solution. The polarizing effect of TAMs was evaluated by flow cytometry, western blot analysis, immunofluorescence staining and in vitro phagocytosis assays. Clinical cervical cancer specimens and an in vivo xenograft model were also employed.

resultsOur previous study showed that hypoxia increased the expression of ZEB1 in cervical squamous cell carcinoma (CSCC) cells, which resulted in increased infiltration of TAMs. Here, we found that hypoxia-induced ZEB1 expression is closely correlated with CD47-SIRPα axis activity in CSCC, which enables cancer cells to evade phagocytosis by macrophages and promotes tumour progression. ZEB1 was found to directly activate the transcription of the CD47 gene in hypoxic CSCC cells. We further showed that endogenous ZEB1 was characteristically enriched in hypoxic CSCC cell-derived exosomes and transferred into macrophages via these exosomes to promote SIRPα

conclusionsOur results suggest that hypoxia-induced ZEB1 promotes immune evasion in CSCC by strengthening the CD47-SIRPα axis. ZEB1-targeted therapy in combination with CD47-SIRPα checkpoint immunotherapy may improve the outcomes of CSCC patients in part by disinhibiting innate immunity.

Indexed as

Carcinoma, Squamous CellTumor EscapeUterine Cervical NeoplasmsZinc Finger E-box-Binding Homeobox 1CD47 AntigenExosomesFemaleHumansImmune EvasionTumor MicroenvironmentCD47 AntigenCD47 protein, humanZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1CD47-SIRPα axisCervical cancerExosomeHypoxiaImmune evasion

Identifiers

PMID38183060
PMCPMC10768116
OpenAlexW4390613285

What OpenQuestion holds

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LicenceCC BY
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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.