Evidence map›Paper›PMID 24858042›Full record

ArticleOncogene2015

Epithelial-mesenchymal status renders differential responses to cisplatin in ovarian cancer.

Q H Miow, T Z Tan, J Ye, J A Lau, T Yokomizo, J-P Thiery, S Mori

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 115 citations in OpenAlex.

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  16. Induction of apoptosis on ovarian adenocarcinoma cells, A2780 by tricyclohexylphosphanegold (I) mercaptobenzoate derivatives via intrinsic and extrinsic pathways.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021
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8 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Q H Miow1] Cancer Science Institute of Singapore, National University of Singapore, Singapore [2] NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.
T Z TanCancer Science Institute of Singapore, National University of Singapore, Singapore.
J YeDean's Office, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
J A LauCancer Science Institute of Singapore, National University of Singapore, Singapore.
T YokomizoDivision of Cancer Genomics, Cancer Institute of Japanese Foundation for Cancer Research, Tokyo, Japan.
J-P Thiery1] Cancer Science Institute of Singapore, National University of Singapore, Singapore [2] Institute of Molecular and Cell Biology, A*STAR, Singapore [3] Department of Biochemistry, National University of Singapore, Singapore.
S Mori1] Cancer Science Institute of Singapore, National University of Singapore, Singapore [2] Division of Cancer Genomics, Cancer Institute of Japanese Foundation for Cancer Research, Tokyo, Japan.
National University of Singapore · SGJapanese Foundation For Cancer Research · JPAgency for Science, Technology and Research · SGNational University Cancer Institute, Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance to platinums, such as cisplatin, is of critical concern in the treatment of ovarian cancer. Recent evidence has linked epithelial-mesenchymal transition (EMT) as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin and EMT in ovarian cancer. Expression microarrays were utilized to estimate the EMT status as a binary phenotype, and the transcriptional responses of 46 ovarian cancer cell lines to cisplatin were measured at dosages equivalent to 50% growth inhibition. Phenotypic responses to cisplatin were quantified with respect to cell number, proliferation rate and apoptosis, and then compared with the epithelial or mesenchymal status. Ovarian cancer cell lines with an epithelial status exhibited higher resistance to cisplatin treatment in the MTS assay than those with a mesenchymal status. Pathway analyses revealed the induction of G1/S- and S-phase genes (P=0.001) and the activation of multiple NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) downstream genes (P=0.0016) by cisplatin selectively in epithelial-like cell lines. BrdU incorporation and Caspase-3/7 release assays confirmed impaired apoptosis in epithelial-like ovarian cancer cells. In clinical samples, we observed resistance to single platinum treatment and the selective activation of the NF-κB pathway by platinum in ovarian cancers with an epithelial status. Overall, our results suggest that, in epithelial-like ovarian cancer cells, NF-κB activation by cisplatin may lead to defective apoptosis, preferential proliferation arrest and a consequential decreased sensitivity to cisplatin.

Indexed as

Antineoplastic AgentsCarcinoma, Ovarian EpithelialCell Line, TumorCisplatinDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHumansNeoplasms, Glandular and EpithelialNF-kappa BOvarian NeoplasmsAntineoplastic AgentsCisplatinNF-kappa B

Identifiers

PMID24858042
OpenAlexW2079484912

What OpenQuestion holds

Textmetadata
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.