Evidence map›Paper›PMID 34422627›Full record

ArticleFrontiers in oncology2021

CXCL10 Produced by HPV-Positive Cervical Cancer Cells Stimulates Exosomal PDL1 Expression by Fibroblasts

Xiaona Chen, Hui He, Yue Xiao, Ayshamgul Hasim, Jianlin Yuan, Min Ye, Xin Li, Yi Hao, Xia Guo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  11. Development of DPP-4-resistant CXCL9-Fc and CXCL10-Fc chemokines for effective cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 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

9 authors at 4 institutions in 2 countries.

Xiaona ChenCenter for Clinical Research and Innovation (CCRI), Shenzhen Hospital, Southern Medical University, The Third School of Clinical Medicine, Southern Medical University, Shenzhen, China.
Hui HeDepartment of Pathology, Shenzhen Hospital, The University of Hong Kong, Shenzhen, China.
Yue XiaoCenter for Clinical Research and Innovation (CCRI), Shenzhen Hospital, Southern Medical University, The Third School of Clinical Medicine, Southern Medical University, Shenzhen, China.
Ayshamgul HasimDepartment of Pathology, Basic College, Xinjiang Medical University, Urumqi, China.
Jianlin YuanDepartment of Gynecology, Affiliated Cancer Hospital, Xinjiang Medical University, Urumqi, China.
Min YeDepartment of Pathology, Affiliated Cancer Hospital, Xinjiang Medical University, Urumqi, China.
Xin LiCenter for Clinical Research and Innovation (CCRI), Shenzhen Hospital, Southern Medical University, The Third School of Clinical Medicine, Southern Medical University, Shenzhen, China.
Yi HaoDepartment of Ultrasound, South China Hospital of Shenzhen University, Shenzhen, China.
Xia GuoCenter for Clinical Research and Innovation (CCRI), Shenzhen Hospital, Southern Medical University, The Third School of Clinical Medicine, Southern Medical University, Shenzhen, China.
Southern Medical University Shenzhen Hospital · CNXinjiang Medical University · CNShenzhen University · CNUniversity of Hong Kong - Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent infection with human papillomavirus (HPV) and immune surveillance failure may be the initiating factors for the carcinogenesis of cervical squamous cell carcinoma (CSCC). HPV infection might affect the innate immune pathway of cervical epithelial cells that constitute the "microenvironment" for tumor cells. Programmed death-ligand 1 (PD-L1) has been reported to be an immunosuppressor that helps cancer cells escape the actions of T cells. In the present study, CXCL10 was substantially upregulated both in cervical tissues of HPV infected patients with cervical intraepithelial neoplasia (CIN) or CSCC, as well as in HPV16 E6/E7 transgenic murine cervix. The HPV-positive (HPV+) cervical cancer cell lines SiHa and Caski secreted increased levels of CXCL10 compared to human foreskin fibroblasts (HFF-1), and its receptor CXCR3 was overexpressed in HFF-1. After co-culture with SiHa or Caski, the JAK-STAT signaling pathway and exosomal PD-L1 expression were both upregulated in HFF-1. Recombinant human CXCL10 induced JAK-STAT and PD-L1, while the CXCL10-CXCR3 and JAK-STAT inhibitors AMG487 or ruxolitinib reduced the expression of PD-L1 in HFF-1 cells. Furthermore, the upregulated expression of PD-L1 was verified in HPV+ but not HPV-negative (HPV-) patients with cervical cancers by analysis of tissue microarray cores in 25 cervical lesion patients (

Indexed as

cervical cancerCXCL10-CXCR3 axishuman papillary virusinnate and adaptive immune responses pathwaysJAK-STATPD-L1TLR signaling pathways

Identifiers

PMID34422627
PMCPMC8377428
OpenAlexW3192070032

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.