Evidence map›Paper›PMID 35142593›Full record

ArticleBioengineered2022

Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model.

Xin Pan, Minxiao Yi, Chaofan Liu, Yu Jin, Bo Liu, Guangyuan Hu, Xianglin Yuan

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 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

7 authors at 1 institution in 1 country.

Xin PanDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Minxiao YiDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0001-7957-2244
Chaofan LiuDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0001-6181-7012
Yu JinDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0002-3427-4937
Bo LiuDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0001-5118-1890
Guangyuan HuDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0002-8060-4917
Xianglin YuanDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0003-4653-5388
Tongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrins play an important role in multiple stages of tumor progression and metastasis. Previous studies have shown synergistic effects of combined αvβ6-integrin and αvβ8-integrin inhibitors with immunotherapy. However, the role of αvβ3-integrin inhibitor in tumor immunity is still unclear. In this study, we aimed to elucidate the impact of the αvβ3-integrin inhibitor on PD-L1 expression and sensitivity to immune checkpoint blockade in melanoma. We investigated the effects of cilengitide, an αvβ3-integrin inhibitor, on cell viability and apoptosis of melanoma cell lines. And we explored how cilengitide regulated the expression of PD-L1 in melanoma cells in vitro and in vivo, using immunofluorescence, flow cytometry, Western blotting, and immunohistochemistry. A subcutaneous B16 murine melanoma model was utilized to determine whether combining cilengitide with anti-PD1 therapy inhibited tumor growth and positively regulated tumor microenvironment (TME). Our results showed that cilengitide inhibited cell viability and induced apoptosis in B16 and A375 cell lines. Furthermore, cilengitide decreased PD-L1 expression by reducing STAT3 phosphorylation in two melanoma cell lines. Cilengitide also reduced subcutaneous tumor PD-L1 expression in the B16 murine melanoma model. Accordingly, cilengitide positively regulated antitumor immune responses and provided durable therapy when combined with anti-PD1 monoclonal antibody in the murine melanoma model. This combination therapy reduced tumor growth and extended survival. Our study highlights that cilengitide enhances the efficacy of anti-PD1 therapy and produces a stronger antitumor immune response. This combination therefore represents a novel therapeutic regimen that may improve immunotherapy treratment.

Indexed as

AnimalsApoptosisB7-H1 AntigenCell SurvivalFemaleImmunohistochemistryIntegrin alphaVbeta3Melanoma, ExperimentalMiceMice, Inbred C57BLSkin NeoplasmsSnake VenomsB7-H1 AntigenCd274 protein, mouseCilengitideIntegrin alphaVbeta3Snake Venomscilengitideimmune checkpoint inhibitorMelanomaPD-1 blockadeαvβ3-integrin

Identifiers

PMID35142593
PMCPMC8974133
OpenAlexW4211133980

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.