Evidence map›Paper›PMID 32058648›Full record

ArticleCancer science2020

Exosomes mediate intercellular transfer of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.

Maolin Ge, Zhi Qiao, Yan Kong, Hui Lu, Han Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 29 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

5 authors at 1 institution in 1 country.

Maolin GeState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-8803-1463
Zhi QiaoState Key Laboratory of Microbial Metabolism, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Yan KongSJTU-Yale Joint Center for Biostatistics, Shanghai Jiao Tong University, Shanghai, China.
Hui LuSJTU-Yale Joint Center for Biostatistics, Shanghai Jiao Tong University, Shanghai, China.
Han LiuState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0002-0022-1861
Shanghai Jiao Tong University · CN

Funding

Collaborative Innovation Center of HematologyNational Key Research and Development Program of China 2018YFA0107802National Natural Science Foundation of China 81570119National Natural Science Foundation of China 81973996Program of Shanghai Academic/Technology Research Leader 19XD1402500Samuel Waxman Cancer Research FoundationShanghai Municipal Education Commission Gaofeng Clinical Medicine Grant 20161304Shanghai Municipal Health Commission 2019CXJQ01
6 · The paper itself

Abstract

Proteasome inhibitors significantly improve cancer outcomes, but their use is eventually followed by proteasome inhibitor resistance and relapse. Current understanding of proteasome inhibitor resistance is limited to cell-autonomous mechanisms; whether non-autonomous mechanisms can be implicated in the development of proteasome inhibitor resistance is unclear. Here, we show that proteasome inhibitor tolerance can be transmitted non-autonomously through exosome-mediated intercellular interactions. We revealed that reversible proteasome inhibitor resistance can be transmitted from cells under therapy stress to naïve sensitive cells through exosome-mediated cell cycle arrest and enhanced stemness in mixed-lineage leukemia cells. Integrated multi-omics analysis using the Tied Diffusion through Interacting Events algorithm identified several candidate exosomal proteins that may serve as predictors for proteasome inhibitor resistance and potential therapeutic targets for treating refractory mixed-lineage leukemia. Furthermore, inhibiting the secretion of exosomes is a promising strategy for reversing proteasome inhibitor resistance in vivo, which provides a novel proof of principle for the treatment of other refractory or relapsed cancers.

Indexed as

Cell Line, TumorDrug Resistance, NeoplasmExosomesHumansImmune ToleranceLeukemia, Biphenotypic, AcuteMicroRNAsMolecular Targeted TherapyProteasome Endopeptidase ComplexProteasome InhibitorsMicroRNAsProteasome Endopeptidase ComplexProteasome Inhibitorsdrug toleranceexosomesmixed-lineage leukemianon-autonomousproteasome inhibitor

Identifiers

PMID32058648
PMCPMC7156829
OpenAlexW3006640790

What OpenQuestion holds

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LicenceCC BY-NC
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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.