Evidence map›Paper›PMID 36717670›Full record

ArticleBritish journal of cancer2023

Transcriptome analysis of newly established carboplatin-resistant ovarian cancer cell model reveals genes shared by drug resistance and drug-induced EMT.

Juran Kralj, Margareta Pernar Kovač, Sanja Dabelić, Darija Stupin Polančec, Thorsten Wachtmeister, Karl Köhrer, Anamaria Brozovic

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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 3 institutions in 2 countries.

Juran KraljDivision of Molecular Biology, Ruđer Bošković Institute, Bijenička cesta 54, Zagreb, Croatia.
Margareta Pernar KovačDivision of Molecular Biology, Ruđer Bošković Institute, Bijenička cesta 54, Zagreb, Croatia.
Sanja DabelićDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy and Biochemistry, University of Zagreb, Ante Kovačića 1, Zagreb, Croatia.
Darija Stupin PolančecSelvita, Hondlova ulica 2, 10000, Zagreb, Croatia.
Thorsten WachtmeisterGenomics and Transcriptomics Laboratory at the Biological and Medical Research Center (BMFZ), Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, Düsseldorf, Germany.ORCID 0000-0002-6760-2458
Karl KöhrerGenomics and Transcriptomics Laboratory at the Biological and Medical Research Center (BMFZ), Heinrich-Heine-University Düsseldorf, Universitätsstraße 1, Düsseldorf, Germany.
Anamaria BrozovicDivision of Molecular Biology, Ruđer Bošković Institute, Bijenička cesta 54, Zagreb, Croatia. brozovic@irb.hr.ORCID 0000-0002-6820-2173
Ruđer Bošković Institute · HRHeinrich Heine University Düsseldorf · DEUniversity of Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn ovarian cancer (OC) therapy, even initially responsive patients develop drug resistance.

methodsHere, we present an OC cell model composed of variants with differing degrees of acquired resistance to carboplatin (CBP), cross-resistance to paclitaxel, and CBP-induced metastatic properties (migration and invasion). Transcriptome data were analysed by two approaches identifying differentially expressed genes and CBP sensitivity-correlating genes. The impact of selected genes and signalling pathways on drug resistance and metastatic potential, along with their clinical relevance, was examined by in vitro and in silico approaches.

resultsTMEM200A and PRKAR1B were recognised as potentially involved in both phenomena, also having high predictive and prognostic values for OC patients. CBP-resistant MES-OV CBP8 cells were more sensitive to PI3K/Akt/mTOR pathway inhibitors Rapamycin, Wortmannin, SB216763, and transcription inhibitor Triptolide compared with parental MES-OV cells. When combined with CBP, Rapamycin decreased the sensitivity of parental cells while Triptolide sensitised drug-resistant cells to CBP. Four PI3K/Akt/mTOR inhibitors reduced migration in both cell lines.

conclusionsA newly established research model and two distinct transcriptome analysis approaches identified novel candidate genes enrolled in CBP resistance development and/or CBP-induced EMT and implied that one-gene targeting could be a better approach than signalling pathway inhibition for influencing both phenomena.

Indexed as

Ovarian NeoplasmsProto-Oncogene Proteins c-aktCarboplatinCell Line, TumorDiterpenesDrug Resistance, NeoplasmEpoxy CompoundsFemaleGene Expression ProfilingHumansPhenanthrenesPhosphatidylinositol 3-KinasesSirolimusCarboplatinDiterpenesEpoxy CompoundsPhenanthrenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSirolimustriptolide

Identifiers

PMID36717670
PMCPMC10050213
OpenAlexW4318590614

What OpenQuestion holds

Textmetadata
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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.