Evidence map›Paper›PMID 41895102›Full record

ArticleBrazilian journal of otorhinolaryngology

CXCR4+ cells in NPC tumor sphere have metastatic potential.

Zhenwei Zhu, Jingyu Li, Jingxian Liu, Yuan He, Pei Guo, Kaitai Yao, Lin Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brazilian journal of otorhinolaryngology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Zhenwei ZhuShenzhen Hospital of Southern Medical University, Department of Oncology, Shenzhen, P.R. China; Southern Medical University, School of Basic Medical Sciences, Cancer Research Institute, Key Laboratory of Tumor Immunology Research, Guangzhou, P.R. China.
Jingyu LiSouthern Medical University, Zhujiang Hospital, Department of Pathology, Guangzhou, P.R. China.
Jingxian LiuShenzhen Hospital of Southern Medical University, Department of Oncology, Shenzhen, P.R. China.
Yuan HeUniversity of Science and Technology of China, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Department of Radiation Oncology, Hefei, P.R. China.
Pei GuoShenzhen Hospital of Southern Medical University, Department of Pathology, Shenzhen, P.R. China.
Kaitai YaoShenzhen Hospital of Southern Medical University, Department of Oncology, Shenzhen, P.R. China; Southern Medical University, School of Basic Medical Sciences, Cancer Research Institute, Key Laboratory of Tumor Immunology Research, Guangzhou, P.R. China.
Lin ChenSun YatSen University, The First Affiliated Hospital, Department of Pathology, Guangzhou, P.R. China. Electronic address: chenlin67@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNasopharyngeal Carcinoma (NPC) tumor stem cells play a crucial role in the occurrence and development of nasopharyngeal carcinoma, but the identity and role of Cancer Stem Cell (CSC) subpopulations that drive metastasis remain unclear. This study explores the mechanisms of NPC stem cell subpopulations (CXCR4+) in the development of NPC, providing a reference for therapeutic targets for NPC.

methodsImmunohistochemical analysis of CXCR4 expression was performed in 71 NPC and 5 chronic nasopharyngitis tissues. Stemness, tumorigenicity and Epithelial-Mesenchymal Transition (EMT) profiles were established for cells in tumor spheres by flow cytometry (CD133/CXCR4), functional assays, Quantitative Reverse Transcription Polymerase Chain Reaction (RT-qPCR) and Western blotting. CXCR4+ cell metastatic potential was evaluated in a mouse NPC model.

resultsCXCR4 expression correlated with NPC T and N stage. CD133+ and CXCR4+ cells were enriched in the tumor sphere. CXCR4+ subsets had enhanced self-renewal (The CXCR4-positive subgroup exhibited a 45% increase in the ability to form tumor spheres), spindle morphology and migration/invasion with upregulation of markers of EMT, Snail, Twist, Vimentin, N-cadherin, stemness, Oct4, Nanog, Sox2 and downregulation of E-cadherin. CXCR4+ tumorsphere cells potentiated metastatic lung nodules in vivo via SDF-1/CXCR4 signaling, giving a 500% increase relative to controls.

conclusionA metastatic CSC subpopulation present in NPC express CXCR4 and have activated EMT and SDF-1/CXCR4-driven metastasis. CXCR4 may have utility as a biomarker and the SDF-1/CXCR4 axis may be a therapeutic target for NPC.

Indexed as

CarcinomaNasopharyngeal NeoplasmsNeoplastic Stem CellsReceptors, CXCR4AC133 AntigenAnimalsBiomarkers, TumorBlotting, WesternEpithelial-Mesenchymal TransitionFemaleFlow CytometryHumansImmunohistochemistryMaleMiceNasopharyngeal CarcinomaAC133 AntigenBiomarkers, TumorCXCR4 protein, humanReceptors, CXCR4CD133CXCR4/SDF1Epithelial-mesenchymal transitionMetastasisNasopharyngeal carcinoma

Identifiers

PMID41895102
PMCPMC13058973

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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.