Evidence map›Paper›PMID 40520087›Full record

ArticleiScience2025

The Arg/N-degron pathway mediates the secretion of apoptotic exosomes under oxidative stress in cancer cell.

Su Bin Kim, Ji Su Lee, Chan Hoon Jung, Eun Hye Cho, Ho Seok Seo, Gee Eun Lee, Hye Yeon Kim, Su Jin Lee, Min Ju Lee, Hans Jin-Young Oh and 4 more

Abstract read
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Su Bin KimCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Ji Su LeeCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Chan Hoon JungCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Eun Hye ChoCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Ho Seok SeoDepartment of Transdisciplinary Medicine, Seoul National University Hospital, 71 Daehakro, Seoul, Republic of Korea.
Gee Eun LeeCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Hye Yeon KimCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Su Jin LeeCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Min Ju LeeCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Hans Jin-Young OhStructural Genomics Consortium, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Ah Jung HeoGoethe University Frankfurt, Medical Faculty, Institute of Biochemistry II, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.
Do Hyun HanDepartment of Transdisciplinary Medicine, Seoul National University Hospital, 71 Daehakro, Seoul, Republic of Korea.
Yong Tae KwonCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.
Chang Hoon JiCellular Degradation Biology Center and Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul 03080, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes from cancer cells are versatile mediators of cell-to-cell communication, whose cargoes are dynamically loaded in response to various stress conditions. In this study, we demonstrate that under oxidative stress, cancer cells secrete exosomes that induce apoptosis in neighboring cells via the Arg/N-degron pathway. In this mechanism, Rab interacting lysosomal protein (RILP) is cleaved at Asp75 in response to oxidative stress which requires ATE1 R-transferase. The cleaved form of RILP recruits the ESCRT-II proteins VPS22 and VPS36 to endosomes from which the interluminal vesicles are invaginated generating exosomes. By using proteomics analyses, we also demonstrate that exosomes secreted from cancer cells upon oxidative stress are enriched apoptotic proteins including pro-apoptotic and anti-inflammatory cytokine ANXA1. These exosomes induce apoptosis of normal cancer cells transporting ANXA1 in an Arg/N-degron pathway-dependent manner. Our results show that the Arg/N-degron pathway modulates exosome-mediated apoptosis in cancer cells under oxidative stress underlying RILP-dependent secretion of ANXA1.

Indexed as

CancerCell biology

Identifiers

PMID40520087
PMCPMC12167491

What OpenQuestion holds

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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.