Evidence map›Paper›PMID 32855386›Full record

ArticleSignal transduction and targeted therapy2020

Mitomycin C enhanced the efficacy of PD-L1 blockade in non-small cell lung cancer.

Min Luo, Fang Wang, Hong Zhang, Kenneth K W To, Shaocong Wu, Zhen Chen, Shaobo Liang, Liwu Fu

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 52 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

8 authors at 4 institutions in 1 country.

Min LuoState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Fang WangState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Hong ZhangState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Kenneth K W ToSchool of Pharmacy, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong, China.
Shaocong WuState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Zhen ChenState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Shaobo LiangState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China.
Liwu FuState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine; Guangdong Esophageal Cancer Institute, Sun Yat-Sen University Cancer Center, 510060, Guangzhou, China. Fulw@mail.sysu.edu.cn.
Sun Yat-sen University · CNState Key Laboratory of Oncology in South ChinaSun Yat-sen University Cancer Center · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed death ligand 1 (PD-L1) immune checkpoint inhibitors are promising therapeutic agents for treating cancers but the response rate is <20%. Some chemotherapeutic drugs could also activate an anticancer immune response to kill cancer cells, apart from their direct cytotoxicity. Our study investigated the combination of chemotherapeutic drugs with PD-L1 antibody to enhance the response rate of PD-L1 blockade. Non-small cell lung cancer (NSCLC) cells were pre-treated with mitomycin C (MMC) and then co-cultured with peripheral blood mononuclear cells (PBMCs) to investigate the effect of the combination of MMC with PD-L1 antibody. The drug combination was also evaluated in vivo in Lewis lung cancer (LLC) cells-bearing C57BL/6 mice. MMC increased the expressions of PD-L1 and MHC-I in NSCLC cells in vitro and in vivo and enhanced the cytotoxic effect of lymphocytes on NSCLC in vitro. In LLC-bearing mouse model, the combination of MMC and PD-L1 antibody was found to be more effective in retarding tumor growth and prolonging overall survival than either single treatment alone, which was associated with increased lymphocyte infiltration and granzyme B release. Mechanistically, MMC activated the ERK pathway, which subsequently enhanced the binding of c-JUN to the PD-L1 promoter and recruited its co-factor STAT3 to increase PD-L1 expression. The upregulated ERK pathway was shown to activate p65 to increase the MHC-I expression. MMC was shown to enhance the efficacy of PD-L1 blockade in NSCLC cells. Further study is warranted to translate the findings to clinical application.

Indexed as

A549 CellsAntibodies, NeoplasmCarcinoma, Non-Small-Cell LungHumansHuman Umbilical Vein Endothelial CellsLung NeoplasmsMitomycinNeoplasm ProteinsProgrammed Cell Death 1 ReceptorAntibodies, NeoplasmMitomycinNeoplasm ProteinsPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID32855386
PMCPMC7452895
OpenAlexW3081370697

What OpenQuestion holds

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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.