Evidence map›Paper›PMID 29690901›Full record

ArticleBMC cancer2018

CXCL9/10/11, a regulator of PD-L1 expression in gastric cancer.

Chenlu Zhang, Zhi Li, Ling Xu, Xiaofang Che, Ti Wen, Yibo Fan, Ce Li, Shuo Wang, Yu Cheng, Xiaoxun Wang and 2 more

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

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.4field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Chenlu ZhangDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Zhi LiDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Ling XuDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Xiaofang CheDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Ti WenDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Yibo FanDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Ce LiDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Shuo WangDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Yu ChengDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Xiaoxun WangDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China.
Xiujuan QuDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China. xiujuanqu@yahoo.com.ORCID 0000-0002-3135-8772
Yunpeng LiuDepartment of Medical Oncology, the First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, China. cmuliuyunpeng@hotmail.com.
First Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China No.31770963National Natural Science Foundation of China No.81572374National Natural Science Foundation of China NO.81602098National Natural Science Foundation of China No.81673025National Science and Technology Major Project of the Ministry of Science and Technology of China Science NO. 2017ZX09304025Technology Plan Project of Liaoning Province NO.2014226033, 2016007010The General Project of Liaoning province department of education and Distinguished professor of Liaoning Province No.LZ2014037The General Project of Liaoning province department of education and Distinguished professor of Liaoning Province NO.LZ2015073The National Key Research and Development Program of China NO.2017YFC1308900
6 · The paper itself

Abstract

backgroundProgrammed death-ligand 1 (PD-L1) is an immunosuppressor that plays an important role in cancer treatments. Although majority of the studies demonstrated that PD-L1 expression was regulated by cellular intrinsic and extrinsic controls, and IFN-γ was a key molecule of extrinsic control, other studies imply that other cytokines play important roles in PD-L1 expression. In this study, we investigated the regulation of PD-L1 by chemokine signaling pathway in gastric cancer (GC) cells.

methodsBioinformatics was used to explore the PD-L1-related genes in GC and propose a hypothesis. PD-L1 and CXCR3 expression were detected by western blot in SGC7901 and MKN74 cell lines. Meanwhile, PD-L1 and CXCR3 expressions were immunohistochemically assessed for their relevance. Moreover, PD-L1, pSTAT3 and pAkt were detected after treatment with CXCL9/10/11. Furthermore,PD-L1, pSTAT3 and pAkt were evaluated after blocking chemokine signaling in SGC7901 cells.

resultsBased on online database analysis, CXCL9/10/11-CXCR3 is proposed to upregulate PD-L1 expression by activating the STAT and PI3K-Akt pathways. This hypothesis was confirmed by in vitro and vivo experiments. CXCR3 and PD-L1 were expressed in GC cell lines and tissues, and the expression of CXCR3 and PD-L1 was positively related. PD-L1 was upregulated after treatment with CXCL9/10/11, accompanied by activation of STAT3 and Akt. After blocking chemokine signaling, upregulation of PD-L1 and activation of STAT3 and Akt were diminished.

conclusionsCXCL9/10/11-CXCR3 upregulated the expression of PD-L1 by activating the STAT and PI3K-Akt signaling pathways in GC cells. There was a significant positive correlation between the expression of PD-L1 and CXCR3 in gastric cancer patient tissues.

Indexed as

Gene Expression Regulation, NeoplasticB7-H1 AntigenBiomarkersCell Line, TumorChemokine CXCL10Chemokine CXCL11Chemokine CXCL9Chemokines, CXCComputational BiologyHumansImmunohistochemistryMolecular Sequence AnnotationNeoplasm StagingPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR3B7-H1 AntigenBiomarkersCD274 protein, humanChemokine CXCL10Chemokine CXCL11Chemokine CXCL9Chemokines, CXCCXCL9 protein, humanCXCR3 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CXCR3STAT3 Transcription FactorCXCL9/10/11CXCR3Gastric cancerPD-L1

Identifiers

PMID29690901
PMCPMC5916585
OpenAlexW2805595805

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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.