Evidence map›Paper›PMID 38029455›Full record

ArticleRedox biology2023

Organic Selenium induces ferroptosis in pancreatic cancer cells.

Roberta Noè, Noemi Inglese, Patrizia Romani, Thauan Serafini, Carlotta Paoli, Beatrice Calciolari, Marco Fantuz, Agata Zamborlin, Nicoletta C Surdo, Vittoria Spada and 11 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  10. Mitochondrial Regulation of Ferroptosis in Cancer Cells.International journal of biological sciences · 2025
    Review
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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

21 authors at 7 institutions in 1 country.

Roberta NoèVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Noemi IngleseVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Patrizia RomaniDepartment of Molecular Medicine, University of Padova, 35126, Padova, Italy.
Thauan SerafiniVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy.
Carlotta PaoliVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Beatrice CalciolariVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Marco FantuzVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Agata ZamborlinNEST-Scuola Normale Superiore, 56127, Pisa, Italy; Center for Nanotechnology Innovation, Istituto Italiano di Tecnologia, 56127, Pisa, Italy.
Nicoletta C SurdoVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Neuroscience Institute, National Research Council (CNR), 35121, Padova, Italy.
Vittoria SpadaVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy.
Martina SpacciVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy.
Sara VoltaVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy.
Maria Laura ErminiCenter for Nanotechnology Innovation, Istituto Italiano di Tecnologia, 56127, Pisa, Italy.
Giulietta Di BenedettoVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Neuroscience Institute, National Research Council (CNR), 35121, Padova, Italy.
Valentina FruscaCenter for Nanotechnology Innovation, Istituto Italiano di Tecnologia, 56127, Pisa, Italy; Scuola Superiore Sant'Anna, Piazza Martiri della Libertà 33, 56127, Pisa, Italy.
Claudio SantiGroup of Catalysis and Green Organic Chemistry, Department of Pharmaceutical Sciences, University of Perugia, 06122, Perugia, PG, Italy.
Konstantinos LefkimmiatisVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Molecular Medicine, University of Pavia, Pavia, Italy.
Sirio DupontDepartment of Molecular Medicine, University of Padova, 35126, Padova, Italy.
Valerio VolianiCenter for Nanotechnology Innovation, Istituto Italiano di Tecnologia, 56127, Pisa, Italy; Department of Pharmacy, School of Medical and Pharmaceutical Sciences, University of Genova, 16148, Genoa, Italy. Electronic address: valerio.voliani@unige.it.
Luca SancinetoGroup of Catalysis and Green Organic Chemistry, Department of Pharmaceutical Sciences, University of Perugia, 06122, Perugia, PG, Italy. Electronic address: luca.sancineto@unipg.it.
Alessandro CarrerVeneto Institute of Molecular Medicine (VIMM), 35129, Padova, Italy; Department of Biology, University of Padova, 35126, Padova, Italy. Electronic address: alessandro.carrer@unipd.it.
University of Padua · ITVeneto Institute of Molecular Medicine · ITItalian Institute of Technology · ITUniversity of Perugia · ITScuola Normale Superiore · ITScuola Superiore Sant'Anna · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDA) cells reprogram both mitochondrial and lysosomal functions to support growth. At the same time, this causes significant dishomeostasis of free radicals. While this is compensated by the upregulation of detoxification mechanisms, it also represents a potential vulnerability. Here we demonstrate that PDA cells are sensitive to the inhibition of the mevalonate pathway (MVP), which supports the biosynthesis of critical antioxidant intermediates and protect from ferroptosis. We attacked the susceptibility of PDA cells to ferroptotic death with selenorganic compounds, including dibenzyl diselenide (DBDS) that exhibits potent pro-oxidant properties and inhibits tumor growth in vitro and in vivo. DBDS treatment induces the mobilization of iron from mitochondria enabling uncontrolled lipid peroxidation. Finally, we showed that DBDS and statins act synergistically to promote ferroptosis and provide evidence that combined treatment is a viable strategy to combat PDA.

Indexed as

FerroptosisPancreatic NeoplasmsSelenium4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidHumansLipid PeroxidationPancreas4,4'-dibenzamido-2,2'-stilbenedisulfonic acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidSeleniumDibenzyl diselenide (DBDS)FerroptosisMevalonate pathway (MVP)Pancreatic cancerSelenorganic compounds

Identifiers

PMID38029455
PMCPMC10698006
OpenAlexW4388818923

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.