Evidence map›Paper›PMID 40170164›Full record

ArticleEuropean journal of medical research2025

HPV11E6/E7 induces nasal epithelial hyperplasia through JAK2/STAT3 signaling pathway.

Yi Zhang, Kaisai Tian, Liying Zheng, Gaohan Zhu, Runyu Zhao, Enhui Zhou, Xiaocheng Xue, Shuixian Huang, Xiaoping Chen, Baoji Hu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. [High expression of low-risk hpv in nasal inverted papilloma and its response to interferon therapy].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2026
    Trial
  2. Review
  3. Article
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.

Yi Zhang *School of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China.ORCID http://orcid.org/0000-0003-1539-7322
Kaisai Tian *Department of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0000-0002-2748-8347
Liying Zheng *Department of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0000-0003-2073-4194
Gaohan ZhuSchool of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China.ORCID http://orcid.org/0009-0001-3448-1872
Runyu ZhaoDepartment of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0000-0003-2643-0685
Enhui ZhouDepartment of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0000-0001-8252-7778
Xiaocheng XueDepartment of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0009-0007-3136-4498
Shuixian HuangDepartment of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China.ORCID http://orcid.org/0000-0002-0381-8508
Xiaoping ChenDepartment of Otorhinolaryngology Head and Neck Surgery, Gongli Hospital of Shanghai Pudong New Area, 219 Miao Pu Road, Shanghai, 200135, China. chen_xp2000@163.com.ORCID http://orcid.org/0000-0003-3048-2699
Baoji HuSchool of Gongli Hospital Medical Technology, University of Shanghai for Science and Technology, Shanghai, 200093, China. selfconfidence2005@sina.com.ORCID http://orcid.org/0000-0001-6768-7984
Wenhao YaoDepartment of Otolaryngology Head and Neck Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. wenhao.yao@hotmail.com.ORCID http://orcid.org/0000-0002-2448-3321

Funding

the Clinical Characteristic Subject of Pudong Health Bureau of Shanghai PWYts2021-15the Priority Specialty of Shanghai Pudong Hospital Zdzk2024-07the Shanghai Pudong New Area Science and Technology Development Foundation PKJ2024-Y29
6 · The paper itself

Abstract

objectivesNasal mucosal epithelial hyperplasia can cause nasal hyperplastic diseases, more studies have confirmed that different subtypes of HPV infection play a significant role in nasal proliferative diseases, especially nasal inverted papilloma (NIP). This study aims to elucidate the role and mechanism of the HPV11 subtype in regulating nasal epithelial hyperplasia.

methodsIn our previous study, the expression of HPV infection in NIP was analyzed by Flow-through hybridization and gene chip (HybridMax), with the highest expression rate observed for the HPV11 subtype. Therefore, we aimed to overexpress HPV11E6/E7 in nasal mucosal epithelial cells (HNEpC) to verify the regulatory role and mechanism of HPV11 in nasal epithelial hyperplasia at the cellular level. In this manuscript, we constructed a lentiviral vector overexpressing HPV11E6/E7 and transfected it into HNEpC. We used HNEpC as the control group and HPV11E6/E7-overexpressing cells as the experimental group. Cell proliferation was assessed using CCK-8, EdU, and colony formation assays. Cell migration ability was evaluated by wound healing and Transwell assays. Protein expression levels related to apoptosis, epithelial-mesenchymal transition (EMT), and the JAK2/STAT3 pathway were analyzed by western blot.

resultsThe results showed that overexpression of HPV11E6/E7 significantly increased the proliferation and migration of nasal epithelial cells, promoted the progression of EMT, and inhibited cell apoptosis. Further verification showed that the overexpression of HPV11E6/E7 significantly promoted the activation of the JAK2/STAT3 signaling pathway.

conclusionsIn summary, we found that low-risk subtype HPV11 promotes nasal mucosal epithelial hyperplasia and malignant progression by increasing activation of the JAK2/STAT3 pathway. The JAK2/STAT3 pathway has been prioritized due to its established role in promoting cell proliferation and EMT in HPV-related diseases.

Indexed as

Human papillomavirus 11Janus Kinase 2Nasal MucosaPapillomavirus InfectionsSTAT3 Transcription FactorApoptosisCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansHyperplasiaSignal TransductionJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription FactorEMTHPV11 E6/E7JAK2/STAT3Nasal hyperplastic diseasesNasal inverted papilloma

Identifiers

PMID40170164
PMCPMC11963266

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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.