Evidence map›Paper›PMID 35884493›Full record

ArticleCancers2022

Mitochondrial Elongation and OPA1 Play Crucial Roles during the Stemness Acquisition Process in Pancreatic Ductal Adenocarcinoma.

Cristian Andres Carmona-Carmona, Elisa Dalla Pozza, Giulia Ambrosini, Barbara Cisterna, Marta Palmieri, Ilaria Decimo, José M Cuezva, Emanuela Bottani, Ilaria Dando

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. 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
1.7field-weighted citation impact, top 15% 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, 20 citations in OpenAlex.

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  9. Signaling, cancer cell plasticity, and intratumor heterogeneity.Cell communication and signaling : CCS · 2024
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  11. Article
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  13. Pancreatic cancer stemness: dynamic status in malignant progression.Journal of experimental & clinical cancer research : CR · 2023
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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

9 authors at 2 institutions in 2 countries.

Cristian Andres Carmona-CarmonaDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.ORCID 0000-0003-1412-6512
Elisa Dalla PozzaDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.ORCID 0000-0001-6813-5436
Giulia AmbrosiniDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.ORCID 0000-0003-4210-8610
Barbara CisternaDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.ORCID 0000-0001-9314-4377
Marta PalmieriDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.
Ilaria DecimoSection of Pharmacology, Department of Diagnostics and Public Health, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-6627-1263
José M CuezvaDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), ISCIII and Instituto de Investigación Hospital 12 de Octubre, Universidad Autónoma de Madrid, 28049 Madrid, Spain.ORCID 0000-0003-1118-248X
Emanuela BottaniSection of Pharmacology, Department of Diagnostics and Public Health, University of Verona, 37134 Verona, Italy.ORCID 0000-0003-1217-8722
Ilaria DandoDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-6390-4184
University of Verona · ITConsejo Superior de Investigaciones Científicas · ES

Funding

INVITE project has received funding from the European Union's Horizon 2020 research and innova-tion programme under the Marie Skłodowska-Curie grant agreement No. 754345. 754345Ministero Dell'Istruzione e della Ricerca N/A
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer with an overall 5-year survival rate of less than 9%. The high aggressiveness of PDAC is linked to the presence of a subpopulation of cancer cells with a greater tumorigenic capacity, generically called cancer stem cells (CSCs). CSCs present a heterogeneous metabolic profile that might be supported by an adaptation of mitochondrial function; however, the role of this organelle in the development and maintenance of CSCs remains controversial. To determine the role of mitochondria in CSCs over longer periods, which may reflect more accurately their quiescent state, we studied the mitochondrial physiology in CSCs at short-, medium-, and long-term culture periods. We found that CSCs show a significant increase in mitochondrial mass, more mitochondrial fusion, and higher mRNA expression of genes involved in mitochondrial biogenesis than parental cells. These changes are accompanied by a regulation of the activities of OXPHOS complexes II and IV. Furthermore, the protein OPA1, which is involved in mitochondrial dynamics, is overexpressed in CSCs and modulates the tumorsphere formation. Our findings indicate that CSCs undergo mitochondrial remodeling during the stemness acquisition process, which could be exploited as a promising therapeutic target against pancreatic CSCs.

Indexed as

cancer stem cellsmitochondrial dynamicsmitochondrial fusionOPA1pancreatic ductal adenocarcinoma

Identifiers

PMID35884493
PMCPMC9322438
OpenAlexW4285595658

What OpenQuestion 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 OpenQuestion graph.