Evidence map›Paper›PMID 31449345›Full record

ArticleJournal of cellular and molecular medicine2019

QKI-6 inhibits bladder cancer malignant behaviours through down-regulating E2F3 and NF-κB signalling.

Fei Shi, Zheng Deng, Zheng Zhou, Chen-Yi Jiang, Rui-Zhe Zhao, Feng Sun, Di Cui, Xiao-Yu Bei, Bo-Yu Yang, Qian Sun and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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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

14 authors at 2 institutions in 2 countries.

Fei ShiDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Zheng DengDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Zheng ZhouDepartment of Urology, Shanghai General Hospital Affiliated to Nanjing Medical University, Shanghai, China.
Chen-Yi JiangDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Rui-Zhe ZhaoDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Feng SunDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Di CuiDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Xiao-Yu BeiDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Bo-Yu YangDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Qian SunDepartment of Urology, Shanghai General Hospital Affiliated to Nanjing Medical University, Shanghai, China.
Xing-Jie WangDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Qi WuDepartment of Urology, Shanghai General Hospital Affiliated to Nanjing Medical University, Shanghai, China.
Shu-Jie XiaDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Bang-Min HanDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0001-9101-8377
Shanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quaking homolog (QKI) is a member of the RNA-binding signal transduction and activator of proteins family. Previous studies showed that QKI possesses the tumour suppressor activity in human cancers by interacting with the 3'-untraslated region (3'-UTR) of various gene transcripts via the STAR domain. This study first assessed the association of QKI-6 expression with clinicopathological and survival data from bladder cancer patients and then investigated the underlying molecular mechanisms. Bladder cancer tissues (n = 223) were subjected to immunohistochemistry, and tumour cell lines and nude mice were used for different in vitro and in vivo assays following QKI-6 overexpression or knockdown. QKI-6 down-regulation was associated with advanced tumour TNM stages and poor patient overall survival. QKI-6 overexpression inhibited bladder cancer cell growth and invasion capacity, but induced tumour cell apoptosis and cell cycle arrest. Furthermore, ectopic expression of QKI-6 reduced tumour xenograft growth and expression of proliferation markers, Ki67 and PCNA. However, knockdown of QKI-6 expression had opposite effects in vitro and in vivo. QKI-6 inhibited expression of E2 transcription factor 3 (E2F3) by directly binding to the E2F3 3'-UTR, whereas E2F3 induced QKI-6 transcription by binding to the QKI-6 promoter in negative feedback mechanism. QKI-6 expression also suppressed activity and expression of nuclear factor-κB (NF-κB) signalling proteins in vitro, implying a novel multilevel regulatory network downstream of QKI-6. In conclusion, QKI-6 down-regulation contributes to bladder cancer development and progression.

Indexed as

3' Untranslated RegionsAnimalsApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDown-RegulationE2F3 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansKi-67 AntigenMaleMiceMice, Nude3' Untranslated RegionsE2F3 protein, humanE2F3 Transcription FactorKi-67 AntigenMKI67 protein, humanNF-kappa BPCNA protein, humanProliferating Cell Nuclear AntigenQKI protein, humanRNA-Binding Proteinsbladder cancerE2F3gene regulationQKIsurvivaltumour progression

Identifiers

PMID31449345
PMCPMC6787450
OpenAlexW2970065934

What OpenQuestion holds

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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.