Evidence map›Paper›PMID 41833656›Full record

ArticleCancer letters2026

Autophagy is essential for survival and function of polyploid giant cancer cells under therapeutic stress.

D Ghosh, B White, X Lu, M Perricone, M Zhou, B Xuan, Y Li, Y Wang, M R Dawson

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2026. 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. Review
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

9 authors.

D GhoshDepartment of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI, 02912, USA.
B WhiteSchool of Engineering, Brown University, Providence, RI, 02912, USA; Institute for Biology, Engineering and Medicine, Brown University, Providence, RI, 02912, USA.
X LuSchool of Engineering, Brown University, Providence, RI, 02912, USA; Institute for Biology, Engineering and Medicine, Brown University, Providence, RI, 02912, USA.
M PerriconeBrown University, Providence, RI, 02912, USA.
M ZhouSchool of Engineering, Brown University, Providence, RI, 02912, USA; Institute for Biology, Engineering and Medicine, Brown University, Providence, RI, 02912, USA.
B XuanBrown University, Providence, RI, 02912, USA.
Y LiBrown University, Providence, RI, 02912, USA.
Y WangDepartment of Pathology and Laboratory Medicine, Brown University, Providence, RI, 02912, USA.
M R DawsonDepartment of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI, 02912, USA; School of Engineering, Brown University, Providence, RI, 02912, USA; Institute for Biology, Engineering and Medicine, Brown University, Providence, RI, 02912, USA. Electronic address: michelle_dawson@brown.edu.

Funding

Lipid Metabolism Switch Triggers Invasive and Chemoresistant Epithelial Ovarian Cancer PhenotypeR01CA266415 · NCI · BROWN UNIVERSITY · PI DAWSON, MICHELLE R · 2022 to 2025
$1.8M
NCI NIH HHS R01 CA266415
6 · The paper itself

Abstract

Polyploid giant cancer cells (PGCCs) are enlarged, multinucleated tumor cells that arise in response to stressors such as chemotherapy and are increasingly recognized as key drivers of recurrence and metastasis in aggressive cancers. Found in triple-negative breast cancer (TNBC) and ovarian cancer (OC), PGCCs can survive cytotoxic therapy in a dormant state and later produce chemoresistant progeny through amitotic budding. Here, we investigated the role of autophagy in paclitaxel (PTX)-induced PGCC survival, nuclear maintenance, and migration. PGCCs generated from MDA-MB-231 and HEY cells were significantly larger, more heterogeneous, and more resistant to PTX than parent cells. Transcriptomic profiling revealed enrichment of metabolic and cytoskeletal pathways, with strong upregulation of autophagy-related genes, including SQSTM1 (P62), LC3, and LAMP1. PGCCs exhibited elevated oxidative stress and marked induction of mitochondrial superoxide dismutase 2 (SOD2). p62 was localized near micronuclei, and prolonged autophagy inhibition with Bafilomycin A1 reduced nuclear size, heterogeneity, and micronuclei number. PGCCs also displayed a dispersed vimentin intermediate filament network that scaffolded autophagic structures; autophagy inhibition impaired migration in PGCC-derived daughter cells. These findings identify autophagy as a critical process sustaining PGCC survival, structural integrity, and motility, and suggest that targeting autophagy may disrupt PGCC-driven recurrence in aggressive cancers.

Indexed as

AutophagyOvarian NeoplasmsPaclitaxelPolyploidyAntineoplastic Agents, PhytogenicCell Line, TumorCell MovementCell SurvivalDrug Resistance, NeoplasmFemaleHumansMDA-MB-231 CellsOxidative StressAntineoplastic Agents, PhytogenicPaclitaxelAutophagyDaughter cellsMicronucleip62PaclitaxelPGCCVimentin

Identifiers

PMID41833656
PMCPMC13455339

What Socratic holds

Textmetadata
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 Socratic graph.