Evidence map›Paper›PMID 37075122›Full record

ArticleScience advances2023

Autophagy supports mitochondrial metabolism through the regulation of iron homeostasis in pancreatic cancer.

Subhadip Mukhopadhyay, Joel Encarnación-Rosado, Elaine Y Lin, Albert S W Sohn, Huan Zhang, Joseph D Mancias, Alec C Kimmelman

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 61 citations in OpenAlex.

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  20. Important molecular mechanisms in ferroptosis.Molecular and cellular biochemistry · 2025
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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

7 authors at 2 institutions in 1 country.

Subhadip MukhopadhyayDepartment of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Grossman School of Medicine, New York, NY 10016, USA.ORCID 0000-0002-7025-8694
Joel Encarnación-RosadoDepartment of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Grossman School of Medicine, New York, NY 10016, USA.ORCID 0000-0002-0440-4278
Elaine Y LinDepartment of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Grossman School of Medicine, New York, NY 10016, USA.ORCID 0000-0003-3057-4163
Albert S W SohnDepartment of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Grossman School of Medicine, New York, NY 10016, USA.ORCID 0000-0001-7869-4362
Huan ZhangDivision of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
Joseph D ManciasDivision of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-0692-3717
Alec C KimmelmanDepartment of Radiation Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Grossman School of Medicine, New York, NY 10016, USA.ORCID 0009-0002-9465-8411
New York University · USDana-Farber Cancer Institute · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1M
The RAS and P13K Pathways in Pancreatic AdenocarcinomaP01CA117969 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2006 to 2025
$41.7M
Identifying Metabolic Dependencies of Pancreatic CancersR35CA232124 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KIMMELMAN, ALEC · 2018 to 2024
$6.5M
Targeting the autophagy-lysosome system to block pancreatic cancerR01CA251726 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PERERA, RUSHIKA MIRIAM · 2021 to 2025
$1.8M
NCI NIH HHS P01 CA117969NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA251726NCI NIH HHS R35 CA232124
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) cells maintain a high level of autophagy, allowing them to thrive in an austere microenvironment. However, the processes through which autophagy promotes PDAC growth and survival are still not fully understood. Here, we show that autophagy inhibition in PDAC alters mitochondrial function by losing succinate dehydrogenase complex iron sulfur subunit B expression by limiting the availability of the labile iron pool. PDAC uses autophagy to maintain iron homeostasis, while other tumor types assessed require macropinocytosis, with autophagy being dispensable. We observed that cancer-associated fibroblasts can provide bioavailable iron to PDAC cells, promoting resistance to autophagy ablation. To overcome this cross-talk, we used a low-iron diet and demonstrated that this augmented the response to autophagy inhibition therapy in PDAC-bearing mice. Our work highlights a critical link between autophagy, iron metabolism, and mitochondrial function that may have implications for PDAC progression.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsAutophagyCell Line, TumorHomeostasisMiceMitochondriaTumor Microenvironment

Identifiers

PMID37075122
PMCPMC10115412
OpenAlexW4366449373

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.