Evidence map›Paper›PMID 28060741›Full record

ArticleOncotarget2017

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways.

Dexin Yu, Hao Geng, Zhiqi Liu, Li Zhao, Zhaofeng Liang, Zhiqiang Zhang, Dongdong Xie, Yi Wang, Tao Zhang, Jie Min and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  10. Mutational Landscape and Environmental Effects in Bladder Cancer.International journal of molecular sciences · 2020
    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

11 authors at 4 institutions in 1 country.

Dexin YuDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Hao GengDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Zhiqi LiuDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Li ZhaoDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Zhaofeng LiangDepartment of Preventive Medicine and Public Health Laboratory Sciences, School of Medicine, Jiangsu University, Jiangsu 212013, China.
Zhiqiang ZhangDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Dongdong XieDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Yi WangDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Tao ZhangDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Jie MinDepartment of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei 230032, China.
Caiyun ZhongDepartment of Toxicology and Nutritional Science, School of Public Health, Nanjing Medical University, Nanjing 210029, China.
Anhui Medical University · CNSecond Hospital of Anhui Medical University · CNJiangsu University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoke has been shown to be a major risk factor for bladder cancer. Epithelial-mesenchymal transition (EMT) is a crucial process in cancer development. The role of MAPK pathways in regulating cigarette smoke-triggered urocystic EMT remains to be elucidated. Human normal urothelial cells and BALB/c mice were used as in vitro and in vivo cigarette smoke exposure models. Exposure of human normal urothelial cells to cigarette smoke induced morphological change, enhanced migratory and invasive capacities, reduced epithelial marker expression and increased mesenchymal marker expression, along with the activation of MAPK pathways. Moreover, we revealed that ERK1/2 and p38 inhibitors, but rather JNK inhibitor, effectively attenuated cigarette smoke-induced urocystic EMT. Importantly, the regulatory function of ERK1/2 and p38 pathways in cigarette smoke-triggered urocystic EMT was further confirmed in mice exposed to CS for 12 weeks. These findings could provide new insight into the molecular mechanisms of cigarette smoke-associated bladder cancer development as well as its potential intervention.

Indexed as

AnimalsCell LineCell MovementCell ShapeCigarette SmokingDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHumansInhalation ExposureMaleMice, Inbred BALB Cp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsSignal TransductionSmokeExtracellular Signal-Regulated MAP Kinasesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsSmokebladder cancercigarette smokeepithelial mesenchymal transitionMAPK pathways

Identifiers

PMID28060741
PMCPMC5352442
OpenAlexW2563173141

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.