Evidence map›Paper›PMID 40495204›Full record

ArticleCell communication and signaling : CCS2025

Chemotherapy reprograms miRNA expression profiles in apoptotic extracellular vesicles from medulloblastoma cells, regulating pro- and anti-proliferative effects on recipient drug-naïve cells.

Rosa Mistica C Ignacio, Helen Forgham, Zerong Ma, Anya Jensen, George Sharbeen, Juanfang Ruan, David S Ziegler, Maria Tsoli, Phoebe A Phillips, Chelsea Mayoh and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Rosa Mistica C IgnacioChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Helen ForghamAustralian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, QLD, Australia.
Zerong MaChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Anya JensenChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
George SharbeenPancreatic Cancer Translational Research Group, Adult Cancer Program, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Juanfang RuanElectron Microscope Unit, Mark Wainwright Analytical Centre, UNSW Sydney, Sydney, NSW, Australia.
David S ZieglerChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Maria TsoliChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Phoebe A PhillipsPancreatic Cancer Translational Research Group, Adult Cancer Program, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Chelsea MayohChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Maria KavallarisChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia. m.kavallaris@ccia.unsw.edu.au.
Joshua McCarrollChildren's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia. m.kavallaris@ccia.unsw.edu.au.

Funding

Cancer Australia APP1184840Cancer Institute NSW 2021/CBG0003National Health and Medical Research Council 2017898National Health and Medical Research Council App2002707National Health and Medical Research Council,Australia APP2016464Ross Trust N/A
6 · The paper itself

Abstract

backgroundExtracellular vesicles (EVs) play a crucial role in intercellular communication. While the effects of EVs released from living or non-dying cancer cells are well characterized, the impact of EVs released from chemotherapy-treated or apoptotic cancer cells is less understood. This study investigated the effects of the chemotherapy agent cisplatin on EV release and miRNA content in apoptotic medulloblastoma cells, as well as their influence on the growth of drug-naïve recipient cancer cells.

methodsEVs were isolated from cisplatin-treated and untreated SHH and group 3 medulloblastoma cells, as well as from the blood of mice with orthotopic medulloblastoma tumors. EVs were characterized using nanoparticle tracking analysis, cryo-TEM, and western blotting, and their impact on the growth of recipient medulloblastoma cells in 2D and 3D cultures was assessed. EV-miRNAs were analyzed using small RNA sequencing and qPCR, and the effects of candidate miRNA overexpression on medulloblastoma cell growth and apoptosis were evaluated.

resultsWe demonstrate that apoptotic SHH and group 3 medulloblastoma cells secrete increased numbers of EVs (size range 150-600 nm) both in vitro and in vivo. EVs isolated from cisplatin-treated SHH and group 3 medulloblastoma cells were internalized by recipient medulloblastoma cells and exhibited distinct effects on their growth. EVs from cisplatin-treated SHH medulloblastoma cells reduced clonogenic growth in recipient drug-naïve medulloblastoma cells, whereas EVs from cisplatin-treated group 3 medulloblastoma cells enhanced the clonogenic and sphere-forming capacity of recipient cells. These contrasting effects were associated with significant alterations in EV-miRNA expression profiles between untreated and cisplatin-treated SHH and group 3 medulloblastoma cells. Notably, miR-449a was found to be upregulated in EVs from cisplatin-treated SHH medulloblastoma cells, and its overexpression in medulloblastoma cells led to potent inhibition of growth.

conclusionsOur findings demonstrate, for the first time, that cisplatin-treated medulloblastoma cells from distinct molecular subgroups secrete EVs with altered miRNA expression profiles that either inhibit or promote the growth of recipient cancer cells. This underscores the potential of targeting EV-mediated communication as a novel therapeutic strategy in medulloblastoma.

Indexed as

Antineoplastic AgentsApoptosisCerebellar NeoplasmsCisplatinExtracellular VesiclesGene Expression Regulation, NeoplasticMedulloblastomaMicroRNAsAnimalsCell Line, TumorCell ProliferationHumansMiceAntineoplastic AgentsCisplatinMicroRNAsCisplatinExtracellular vesiclesMedulloblastomaMiRNA

Identifiers

PMID40495204
PMCPMC12150529

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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.