Evidence map›Paper›PMID 30894224›Full record

ArticleBiological research2019

Functional and transcriptomic characterization of carboplatin-resistant A2780 ovarian cancer cell line.

Tamara Viscarra, Kurt Buchegger, Ignacio Jofre, Ismael Riquelme, Louise Zanella, Michel Abanto, Alyssa C Parker, Stephen R Piccolo, Juan Carlos Roa, Carmen Ili and 1 more

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Harnessing preclinical models for the interrogation of ovarian cancer.Journal of experimental & clinical cancer research : CR · 2022
    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

11 authors at 4 institutions in 2 countries.

Tamara ViscarraLaboratorio de Patología Molecular, Centro de Excelencia en Medicina Traslacional-Scientific and Technological Bioresource Nucleus (CEMT-BIOREN), Universidad de La Frontera, Avenida Alemania #0478, 3th Floor, Temuco, Chile.
Kurt BucheggerLaboratorio de Patología Molecular, Centro de Excelencia en Medicina Traslacional-Scientific and Technological Bioresource Nucleus (CEMT-BIOREN), Universidad de La Frontera, Avenida Alemania #0478, 3th Floor, Temuco, Chile.
Ignacio JofreLaboratory of Neurosciences and Biological Peptides, Center of Biotechnology in Reproduction (CEBIOR-BIOREN), Department of Preclinical Sciences, Faculty of Medicine, Universidad de La Frontera, Temuco, Chile.
Ismael RiquelmeInstituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Temuco, Chile.
Louise ZanellaLaboratorio de Patología Molecular, Centro de Excelencia en Medicina Traslacional-Scientific and Technological Bioresource Nucleus (CEMT-BIOREN), Universidad de La Frontera, Avenida Alemania #0478, 3th Floor, Temuco, Chile.
Michel AbantoScientific and Technological Bioresource Nucleus (BIOREN), Universidad de La Frontera, Casilla 54-D, Temuco, Chile.
Alyssa C ParkerDepartment of Biology, Brigham Young University, Provo, UT, USA.
Stephen R PiccoloDepartment of Biology, Brigham Young University, Provo, UT, USA.
Juan Carlos RoaDepartment of Pathology, UC Centre for Investigational Oncology (CITO), Advanced Centre for Chronic Diseases (ACCDis), The Millennium Institute on Immunology and Immunotherapy, Pontificia Universidad Católica de Chile, Santiago de Chile, Chile.
Carmen IliLaboratorio de Patología Molecular, Centro de Excelencia en Medicina Traslacional-Scientific and Technological Bioresource Nucleus (CEMT-BIOREN), Universidad de La Frontera, Avenida Alemania #0478, 3th Floor, Temuco, Chile. carmen.ili@ufrontera.cl.
Priscilla BrebiLaboratorio de Patología Molecular, Centro de Excelencia en Medicina Traslacional-Scientific and Technological Bioresource Nucleus (CEMT-BIOREN), Universidad de La Frontera, Avenida Alemania #0478, 3th Floor, Temuco, Chile. brebimieville@gmail.com.
Universidad de La Frontera · CLBrigham Young University · USPontificia Universidad Católica de Chile · CLUniversidad Autónoma de Chile · CL

Funding

Comisión Nacional de Investigación Científica y Tecnológica 21140129Comisión Nacional de Investigación Científica y Tecnológica 21151406Dirección de Investigación, Universidad de La Frontera DI17-0079Fondo Nacional de Desarrollo Científico y Tecnológico 11150622Fondo Nacional de Desarrollo Científico y Tecnológico 11150802Fondo Nacional de Desarrollo Científico y Tecnológico 3170826Fondo Nacional de Desarrollo Científico y Tecnológico 3180550
6 · The paper itself

Abstract

backgroundOvarian cancer is a significant cancer-related cause of death in women worldwide. The most used chemotherapeutic regimen is based on carboplatin (CBDCA). However, CBDCA resistance is the main obstacle to a better prognosis. An in vitro drug-resistant cell model would help in the understanding of molecular mechanisms underlying this drug-resistance phenomenon. The aim of this study was to characterize cellular and molecular changes of induced CBDCA-resistant ovarian cancer cell line A2780.

methodsThe cell selection strategy used in this study was a dose-per-pulse method using a concentration of 100 μM for 2 h. Once 20 cycles of exposure to the drug were completed, the cell cultures showed a resistant phenotype. Then, the ovarian cancer cell line A2780 was grown with 100 μM of CBDCA (CBDCA-resistant cells) or without CBDCA (parental cells). After, a drug sensitivity assay, morphological analyses, cell death assays and a RNA-seq analysis were performed in CBDCA-resistant A2780 cells.

resultsMicroscopy on both parental and CBDCA-resistant A2780 cells showed similar characteristics in morphology and F-actin distribution within cells. In cell-death assays, parental A2780 cells showed a significant increase in phosphatidylserine translocation and caspase-3/7 cleavage compared to CBDCA-resistant A2780 cells (P < 0.05 and P < 0.005, respectively). Cell viability in parental A2780 cells was significantly decreased compared to CBDCA-resistant A2780 cells (P < 0.0005). The RNA-seq analysis showed 156 differentially expressed genes (DEGs) associated mainly to molecular functions.

conclusionCBDCA-resistant A2780 ovarian cancer cells is a reliable model of CBDCA resistance that shows several DEGs involved in molecular functions such as transmembrane activity, protein binding to cell surface receptor and catalytic activity. Also, we found that the Wnt/β-catenin and integrin signaling pathway are the main metabolic pathway dysregulated in CBDCA-resistant A2780 cells.

Indexed as

Antineoplastic AgentsCarboplatinCell DeathCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansOvarian NeoplasmsPhenotypeSequence Analysis, RNASignal TransductionTranscriptomeAntineoplastic AgentsCarboplatinA2780 cell lineCarboplatinDrug resistanceIntegrin signaling pathwayOvarian cancerWnt/β-catenin-signaling pathway

Identifiers

PMID30894224
PMCPMC6427839
OpenAlexW2941574141

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.