Evidence map›Paper›PMID 36658134›Full record

ArticleSignal transduction and targeted therapy2023

Chemo-drugs in cell microparticles reset antitumor activity of macrophages by activating lysosomal P450 and nuclear hnRNPA2B1.

Keke Wei, Huafeng Zhang, Shuaishuai Yang, Yuxiao Cui, Bingxia Zhang, Jincheng Liu, Liang Tang, Yaoyao Tan, Simin Liu, Shiqi Chen and 12 more

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

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  16. Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024
    Review
  17. Review
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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

22 authors.

Keke Wei *Department of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Huafeng Zhang *Department of Pathology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Shuaishuai YangDepartment of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Yuxiao CuiDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Bingxia ZhangCardiovascular Surgery, Union Hospital, Huazhong University of Science & Technology, Wuhan, 430071, China.
Jincheng LiuDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Liang TangDepartment of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Yaoyao TanDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Simin LiuDepartment of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Shiqi ChenCardiovascular Surgery, Union Hospital, Huazhong University of Science & Technology, Wuhan, 430071, China.
Wu YuanDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Xiao LuoDepartment of Pathology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Chen ChenDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Fei LiDepartment of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Junwei LiuCardiovascular Surgery, Union Hospital, Huazhong University of Science & Technology, Wuhan, 430071, China.
Jie ChenDepartment of Immunology & National Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College, Beijing, 100005, China.
Pingwei XuTranslational Medicine Laboratory, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jiadi LvDepartment of Immunology & National Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College, Beijing, 100005, China.
Ke TangDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China.
Yi ZhangBiotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.ORCID 0000-0001-9861-4681
Jingwei MaDepartment of Immunology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China. majingwei@hust.edu.cn.
Bo HuangDepartment of Biochemistry & Molecular Biology, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, 430030, China. tjhuangbo@hotmail.com.ORCID 0000-0001-8476-1138

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages in tumors (tumor-associated macrophages, TAMs), a major population within most tumors, play key homeostatic functions by stimulating angiogenesis, enhancing tumor cell growth, and suppressing antitumor immunity. Resetting TAMs by simple, efficacious and safe approach(s) is highly desirable to enhance antitumor immunity and attenuate tumor cell malignancy. Previously, we used tumor cell-derived microparticles to package chemotherapeutic drugs (drug-MPs), which resulted in a significant treatment outcome in human malignant pleural effusions via neutrophil recruitments, implicating that drug-MPs might reset TAMs, considering the inhibitory effects of M2 macrophages on neutrophil recruitment and activation. Here, we show that drug-MPs can function as an antitumor immunomodulator by resetting TAMs with M1 phenotype and IFN-β release. Mechanistically, drug molecules in tumor MPs activate macrophage lysosomal P450 monooxygenases, resulting in superoxide anion formation, which further amplifies lysosomal ROS production and pH value by activating lysosomal NOX2. Consequently, lysosomal Ca

Indexed as

Antineoplastic AgentsCell-Derived MicroparticlesHeterogeneous-Nuclear Ribonucleoprotein Group A-BMacrophagesCell Line, TumorHumansLysosomesAntineoplastic AgentsHeterogeneous-Nuclear Ribonucleoprotein Group A-BhnRNP A2

Identifiers

PMID36658134
PMCPMC9852455

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.