Evidence map›Paper›PMID 41256627›Full record

ArticlebioRxiv : the preprint server for biology2025

Cancer cells surviving cisplatin chemotherapy increase stress-induced OMA1 activity and mitochondrial fragmentation.

Melvin Li, Chenille A McCullum, Louis T A Rolle, Qin Ni, Zhuoxu Ge, Sean X Sun, Kenneth J Pienta, Sarah R Amend

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

5 · Who and what money

Authors and funding

8 authors.

Melvin LiCancer Ecology Center, The James Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Chenille A McCullumCancer Ecology Center, The James Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Louis T A RolleCancer Ecology Center, The James Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Qin NiInstitute for NanoBio Technology, Johns Hopkins University.
Zhuoxu GeInstitute for NanoBio Technology, Johns Hopkins University.
Sean X SunInstitute for NanoBio Technology, Johns Hopkins University.
Kenneth J PientaCancer Ecology Center, The James Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD 21287.
Sarah R AmendCancer Ecology Center, The James Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD 21287.ORCID 0000-0002-5606-1262

Funding

Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KELLER, EVAN T · 2004 to 2024
$29.6M
TRANS_NETWORK PROJECTSU54CA143803 · NCI · PRINCETON UNIVERSITY · PI STURM, JAMES C · 2009 to 2013
$14.2M
Mechanisms That Regulate Dormancy of Disseminated Tumor Cells in the Bone MarrowU54CA163124 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHIOZAWA, YUSUKE · 2011 to 2015
$3.0M
Reactive Stroma and Tumor Associated Macrophages in Prostate Cancer ProgressionU01CA143055 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIENTA, KENNETH J., ROWLEY, DAVID R · 2010 to 2014
$2.7M
LSM880 Laser-scanning Microscope with Airyscan ModuleS10OD023548 · OD · JOHNS HOPKINS UNIVERSITY · PI KUO, SCOT CHARLES · 2018 to 2018
$439k
NCI NIH HHS P01 CA093900NCI NIH HHS U01 CA143055NCI NIH HHS U54 CA143803NCI NIH HHS U54 CA163124NIH HHS S10 OD023548
6 · The paper itself

Abstract

Cancer is one of the leading causes of deaths worldwide. Once cancer acquires therapy resistance, it becomes the main driver of cancer lethality in patients. Thus, mechanisms of therapy resistance must be investigated to improve patient outcomes. Mitochondria are critical organelles in the cellular stress responses, undergoing dynamic morphological and functional changes in response to external stimuli. We and others have identified a chemotherapy-resistant cancer cell state where cells that survive treatment exhibit a dramatic increase in cell size and remain non-proliferative for weeks. In this study, we demonstrate that cancer cells that enter this resistant cell state in response to cisplatin increase OMA1 activity and decrease mitochondrial fusion and function to combat oxidative stress. These findings contribute to further understanding the role of the mitochondrial stress responses in therapy resistance in cancer and provide a potential therapeutic avenue to targeting cancer cells that enter this chemotherapy-resistant cell state.

Indexed as

cancermitochondrial dynamicsmitochondrial morphologyOMA1OPA1oxidative stress

Identifiers

PMID41256627
PMCPMC12622012

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.