Evidence map›Paper›PMID 27391066›Full record

ArticleOncotarget2016

miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression.

Xiaolu Cui, Chuize Kong, Yuyan Zhu, Yu Zeng, Zhe Zhang, Xiankui Liu, Bo Zhan, Chiyuan Piao, Zhenming Jiang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. MicroRNA-130b functions as an oncogene and is a predictive marker of poor prognosis in lung adenocarcinoma.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. MicroRNAs: Key Players in Bladder Cancer.Molecular diagnosis & therapy · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Xiaolu CuiDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Chuize KongDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Yuyan ZhuDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Yu ZengDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Zhe ZhangDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Xiankui LiuDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Bo ZhanDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Chiyuan PiaoDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Zhenming JiangDepartment of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent activation of NF-κB signaling is closely related to chronic inflammation and tumorigenesis. Commonly, NF-κB signaling is tightly controlled by multiple feedback loops and regulators, such as the deubiquitinases (DUBs). However, in cancer cells, NF-κB may override these feedbacks through special pathways and lead to the sustained activation. In the present study, we demonstrate that in transitional cell carcinoma (TCC) of bladder, miR-130b plays an oncogenesis role, it enhanced proliferation, invasion and migration of TCC cell, and was highly correlated with tumor progression. On the other hand, NF-κB directly regulated the transcription of miR-130b by binding with its promoter region. Importantly, we verify that, through deceasing the expression of Cylindromatosis (CYLD), a K63-specific DUB and endogenous blocker of NF-κB signaling, miR-130b can in return sustain the persistent activation of NF-κB, which may promote the malignant progression of TCC. Thus, the present study uncovers a potential signaling transduction in which NF-κB is continuously activated, and may provide a novel therapeutic approach for the clinical management of TCC.

Indexed as

Gene Expression Regulation, NeoplasticAgedAnimalsCarcinogenesisCarcinoma, Transitional CellCell Line, TumorCell ProliferationDeubiquitinating Enzyme CYLDDisease ProgressionFemaleHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsCYLD protein, humanDeubiquitinating Enzyme CYLDMicroRNAsMIRN130 microRNA, humanNF-kappa Bbladder transitional cell carcinomaCYLDmiR-130bNF-κB

Identifiers

PMID27391066
PMCPMC5217037
OpenAlexW2473118538

What OpenQuestion holds

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LicenceCC BY
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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.