Evidence map›Paper›PMID 31234823›Full record

ArticleBMC cancer2019

Inhibition of PI3K/Akt/mTOR signaling pathway alleviates ovarian cancer chemoresistance through reversing epithelial-mesenchymal transition and decreasing cancer stem cell marker expression.

Junli Deng, Xupeng Bai, Xiaojie Feng, Jie Ni, Julia Beretov, Peter Graham, Yong Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 1 pooled it
12.2field-weighted citation impact, top 1% 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

159 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.

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99 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.

Junli DengCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Xupeng BaiCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Xiaojie FengCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Jie NiCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Julia BeretovCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Peter GrahamCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia.
Yong LiCancer Care Centre, St George Hospital, 4-10 South St, Kogarah, NSW, 2217, Australia. y.li@unsw.edu.au.
St George Hospital · AUSutherland Hospital · AUUNSW Sydney · AUHenan Cancer Hospital · CN

Funding

China Sponsorship Council N/A
6 · The paper itself

Abstract

backgroundOvarian cancer is the most common malignant tumor of the female reproductive tract. Chemoresistance is a major challenge for current ovarian cancer therapy. However, the mechanism underlying epithelial ovarian cancer (EOC) chemoresistance is not completely uncovered. The phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is an important intracellular pathway in regulating cell cycle, quiescence, and proliferation. The aim of this study is to investigate the role of PI3K/Akt/mTOR signaling pathway and its association with epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) marker expression in EOC chemoresistance.

methodsThe expressions of EMT and CSC markers were detected by immunofluorescence, western blot, and quantitative real-time PCR. BEZ235, a dual PI3K/mTOR inhibitor, was employed to investigate the role of PI3K/Akt/ mTOR signaling in regulating EMT and CSC marker expression. Students' t test and one-way ANOVA with Tukey's post-hoc test were used to compare the data from different groups.

resultsWe found that EMT and CSC marker expression were significantly enhanced in chemoresistant EOC cells, which was accompanied by the activation of PI3K/Akt/mTOR signaling. Compared with single cisplatin treatment, combined treatment with BEZ235 and cisplatin significantly disrupted the colony formation ability, induced higher ROS level and more apoptosis in chemoresistant EOC cells. Furthermore, the combination approach effectively inhibited PI3K/Akt/mTOR signaling pathway, reversed EMT, and decreased CSC marker expression in chemoresistant EOC cells compared with cisplatin mono-treatment.

conclusionsOur results first demonstrate that EMT and enhanced CSC marker expression triggered by activated PI3K/Akt/mTOR signaling are involved in the chemoresistance of EOC, and BEZ235 in combination with cisplatin might be a promising treatment option to reverse EOC chemoresistance.

Indexed as

Analysis of VarianceApoptosisCarcinoma, Ovarian EpithelialCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHumansImidazolesNeoplastic Stem CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinolinesReactive Oxygen SpeciesCisplatindactolisibImidazolesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinolinesReactive Oxygen SpeciesTOR Serine-Threonine KinasesChemoresistanceCSCEMTOvarian cancerPI3K/Akt/mTOR signaling

Identifiers

PMID31234823
PMCPMC6591840
OpenAlexW2952074268

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.