Evidence map›Paper›PMID 36434587›Full record

ArticleBMC urology2022

NEAT1 promotes the malignant development of bladder cancer by regulating the miR-101/VEGF-C pathway in vitro and in vivo.

Huihui Zhang, Shuang Yu, Kuilin Fei, Zhongxin Huang, Shidong Deng, Hanfeng Xu

Open access · goldAbstract read
In one paragraph

Article in BMC urology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Epigenetic and Immunological Features of Bladder Cancer.International journal of molecular sciences · 2023
    Review
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

6 authors at 3 institutions in 1 country.

Huihui ZhangDepartment of Urology, The First Affiliated Hospital, Hengyang Medical School, University of South China, 69 Chuanshan Road, Hengyang, 421001, Hunan, People's Republic of China.
Shuang YuDepartment of Urology, The People's Hospital of Liuyang, Changsha, 410399, Hunan, People's Republic of China.
Kuilin FeiDepartment of Obstetrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China.
Zhongxin HuangDepartment of Urology, The First Affiliated Hospital, Hengyang Medical School, University of South China, 69 Chuanshan Road, Hengyang, 421001, Hunan, People's Republic of China.
Shidong DengDepartment of Urology, The First Affiliated Hospital, Hengyang Medical School, University of South China, 69 Chuanshan Road, Hengyang, 421001, Hunan, People's Republic of China.
Hanfeng XuDepartment of Urology, The First Affiliated Hospital, Hengyang Medical School, University of South China, 69 Chuanshan Road, Hengyang, 421001, Hunan, People's Republic of China. nanhuaxuhanfeng@126.com.
University of South China · CNHunan Provincial People's Hospital · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNEAT1 has been shown to play an oncogenic role in many kinds of cancers. However, detailed roles of NEAT1 in bladder cancer are largely unknown.

methodsIn the present study, the expression of NEAT1, miR-101 and VEGF-C was detected in human bladder cancer samples. The relationship between NEAT1 and the prognosis of patients with bladder cancer was analysed. In vitro experiments explored the effects of NEAT1 on biological behaviours of bladder cancer T24 and 5637 cells. Bioinformatics prediction and luciferase assays were used to assay the regulatory mechanism of action of NEAT1 and miR-101. Loss and gain of the expression of miR-101 and VEGF-C were used to explore the effects of the NEAT1/miR-101/VEGF-C pathway on T24 and 5637 cells. The effect of NEAT1 on the growth of bladder cancer in vivo was explored using an orthotopic tumourigenesis model.

resultsNEAT1 and VEGF-C were significantly upregulated in bladder cancer samples, and miR-101 was significantly downregulated. NEAT1 upregulation was associated with poorer recurrence-free survival of patients with bladder cancer. Overexpression of NEAT1 promoted the proliferation, migration and invasion of bladder cancer cells. The results of the luciferase assay indicated that miR-101 was a target of NEAT1. The promoting effects of NEAT1 on bladder cancer cells were reversed by miR-101 upregulation, and inhibition of miR-101 enhanced the effects of NEAT1. Overexpression of VEGF-C had a clear synergistic effect with the action of NEAT1. Overexpression of NEAT1 increased tumour growth and induced the development of liver metastasis.

conclusionsIn conclusion, our data indicated that NEAT1 was expressed at high levels in bladder cancer patients and correlated with unfavourable prognosis. NEAT1 promoted malignant development of bladder cancer in vitro and in vivo by regulating the miR-101/VEGF-C pathway.

Indexed as

MicroRNAsRNA, Long NoncodingUrinary Bladder NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansVascular Endothelial Growth Factor CMicroRNAsMIRN101 microRNA, humanRNA, Long NoncodingVascular Endothelial Growth Factor CBladder cancermiR-101NEAT1VEGF-C

Identifiers

PMID36434587
PMCPMC9700885
OpenAlexW4310052640

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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.