Evidence map›Paper›PMID 30845932›Full record

ArticleBMC cancer2019

PPARγ activation serves as therapeutic strategy against bladder cancer via inhibiting PI3K-Akt signaling pathway.

Shidong Lv, Wei Wang, Hongyi Wang, Yongtong Zhu, Chengyong Lei

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 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-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

60 citing papers in PubMed, 120 citations in OpenAlex.

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  18. Associations between Diabetes Mellitus and Selected Cancers.International journal of molecular sciences · 2024
    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

5 authors at 3 institutions in 1 country.

Shidong LvDepartment of Urology, Nanfang Hospital, Southern Medical University, No.1838 North of Guangzhou Avenue, Guangzhou, 510515, China.
Wei WangDepartment of Pathology, General Hospital of Southern Theater Command, PLA, Guangzhou, 510010, China.
Hongyi WangDepartment of Urology, Nanfang Hospital, Southern Medical University, No.1838 North of Guangzhou Avenue, Guangzhou, 510515, China.
Yongtong ZhuDepartment of Obstetrics and Gynecology, Center for Reproductive Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Chengyong LeiDepartment of Urology, Nanfang Hospital, Southern Medical University, No.1838 North of Guangzhou Avenue, Guangzhou, 510515, China. lcy_fimmu@126.com.
Nanfang Hospital · CNGeneral Hospital of Guangzhou Military Command · CNSouthern Medical University · CN

Funding

Guangdong Science and Technology Project 2016ZC0064
6 · The paper itself

Abstract

backgroundHeterogeneity in bladder cancer results in variable clinical outcomes, posing challenges for clinical management of this malignancy. Recent studies suggest both tumor suppressive and oncogenic role of PPARγ in bladder cancer. The fuction of PPARγ signaling pathway in modulating carcinogenesis is controversial.

methodsThe expression of PPARγ and association with overall survival were analyzed in patients from two cohorts. The effect of PPARγ activation on cell proliferation, cell cycle, and cell apoptosis were determined with the agonists (rosiglitazone and pioglitazone), the inverse agonist (T0070907), and the antagonist (GW9662) in Umuc-3 and 5637 bladder cancer cells. The correlation of PPARγ activation with PI3K-Akt pathway was evaluated with RNA sequencing data from the TCGA cases and 30 human bladder cancer cell lines. The effect of PPARγ activation on tumor growth was validated with subcutaneous tumor models in vivo. The effect of PPARγ activation on PI3K-Akt signaling transduction was determined with multiple assays including immunohistochemistry, flow cytometry, proteomic array, and western blotting.

resultsWe showed that PPARγ was a favorable prognostic factor in patients with bladder cancer. PPARγ activation by rosiglitazone and pioglitazone markedly induced cell cycle G2 arrest and apoptosis in bladder cancer cells, which resulted in inhibition of cell proliferation in vitro and suppression of tumor growth in vivo. The underlying mechanism involved marked inhibition of PI3K-Akt pathway.

conclusionsThis study reported the tumor-suppressive effect of PPARγ agonists in bladder cancer, suggesting that transactivation of PPARγ could be served as a potential strategy for the chemoprevention and therapeutic treatment of bladder cancer.

Indexed as

AnimalsApoptosisBiomarkersCell CycleCell Line, TumorCell ProliferationDisease Models, AnimalGene Expression ProfilingHumansImmunohistochemistryMaleMiceModels, BiologicalPhosphatidylinositol 3-KinasesPPAR gammaPrognosisBiomarkersPhosphatidylinositol 3-KinasesPPAR gammaProto-Oncogene Proteins c-aktRosiglitazoneAktApoptosisBladder cancerPI3KPPARγ

Identifiers

PMID30845932
PMCPMC6407222
OpenAlexW2935064944

What OpenQuestion holds

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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.