Evidence map›Paper›PMID 32252184›Full record

ArticleInternational neurourology journal2020

Pioglitazone Alters the Proteomes of Normal Bladder Epithelial Cells but Shows No Tumorigenic Effects.

Muhammad Shahid, Minhyung Kim, Austin Yeon, Peng Jin, Woong-Ki Kim, Sungyong You, Jayoung Kim

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International neurourology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
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 2 institutions in 2 countries.

Muhammad ShahidDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Minhyung KimDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Austin YeonDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Peng JinDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Woong-Ki KimDepartment of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA, USA.
Sungyong YouDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Jayoung KimDepartments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Cedars-Sinai Medical Center · USEastern Virginia Medical School · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
West Coast Central Comprehensive Metabolomics Resource Core (WC3MRC)U24DK097154 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FIEHN, OLIVER · 2012 to 2017
$9.9M
Microbiome and Proteome As Predictive Biomarkers of UCPPSU01DK103260 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI ANGER, JENNIFER TASH, FREEMAN, MICHAEL R · 2014 to 2018
$1.2M
Urinary Metabolites in IC PBS DiagnosisR01DK100974 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI ANGER, JENNIFER TASH, KIM, JAYOUNG · 2013 to 2013
$416k
Centers for Disease Controls and Prevention 1U01DP006079Department of Defense grants W81XWH-15-1-0415 and W81XWH-19-1-0109IMAGINE NO IC Research GrantNational Institutes of Health grants 1U01DK103260, 1R01DK100974, U24 DK097154, NIH NCATS UCLA CTSI UL1TR000124NCATS NIH HHS UL1 TR000124NCCDPHP CDC HHS U01 DP006079NIDDK NIH HHS R01 DK100974NIDDK NIH HHS U01 DK103260NIDDK NIH HHS U24 DK097154Steven Spielberg Discovery FundU.S.-Egypt Science and Technology Joint Fund
6 · The paper itself

Abstract

purposePioglitazone, an antihyperglycemic drug, is widely used in diabetes mellitus patients with insulin resistance. Although pioglitazone is known to have a potential link to bladder cancer (BC), there have been contradictory results. This present study is designed to understand the regulatory mechanisms that drive the effects of pioglitazone on the bladder epithelial cells.

methodsLabeled liquid chromatography-tandem mass spectrometry-based proteomics profiling characterized the global proteomes of normal human bladder epithelial cells treated with or without pioglitazone.

resultsThis approach detected approximately 5,769 proteins in total. Of those 5,769 proteins, 124 were identified as being differentially expressed due to pioglitazone treatment. Further analysis identified 95 upregulated and 29 downregulated proteins (absolute log2 fold change >0.58 and P-value<0.05). The following functional gene enrichment analysis suggested that pioglitazone may be altering a few select biological processes, such as gene/chromatin silencing, by downregulating BMI1 (B lymphoma Mo-MLV insertion region 1 homolog), a polycomb complex protein. Further cell-based assays showed that cell adhesion molecules, epithelial-mesenchymal transition markers, and major signaling pathways were significantly downregulated by pioglitazone treatment.

conclusionThese experimental results revealed the proteomic and biological alterations that occur in normal bladder cells in response to pioglitazone. These findings provided a landscape how bladder proteome is influenced by pioglitazone, which suggests the potential adverse effects of diabetes drugs and their links to bladder dysfunctions.

Indexed as

BMI1Diabetes mellitusGlobal proteomePeroxisome proliferator-activated receptor gammaUrinary bladder neoplasms

Identifiers

PMID32252184
PMCPMC7136443
OpenAlexW3014893023

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.