Evidence map›Paper›PMID 30252587›Full record

ArticleCell cycle (Georgetown, Tex.)2018

Loss of miR-16 contributes to tumor progression by activation of tousled-like kinase 1 in oral squamous cell carcinoma.

Shousen Hu, Honghan Wang, Dan Yan, Wuhao Lu, Pei Gao, Weihua Lou, Xiangzhen Kong

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. The interaction betweenAnnals of medicine · 2023
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Oral Cancer: A Historical Review.International journal of environmental research and public health · 2020
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. 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 3 institutions in 1 country.

Shousen Hua Department of Otolaryngology Head and Neck Surgery , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , China.
Honghan Wangb Department of Head and Neck Surgery, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine , Central South University , Changsha , Hunan , China.
Dan Yanc Department of Pharmacy , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
Wuhao Lua Department of Otolaryngology Head and Neck Surgery , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , China.
Pei Gaoa Department of Otolaryngology Head and Neck Surgery , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , China.
Weihua Loua Department of Otolaryngology Head and Neck Surgery , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , Henan , China.
Xiangzhen Kongc Department of Pharmacy , The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.
First Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A different expression signature of miRNA in oral squamous cell carcinoma (OSCC) has been validated. MicroRNA-16 (miR-16) as one of the distinctly dysregulated miRNAs in OSCC, its functional role in progression of OSCC remains not fully clear. Herein, miR-16 expression was significantly lower in OSCC tissues compared to that in adjacent normal tissues (n = 131). A lower level of miR-16 was found to be associated with poor prognosis on a cohort of 131 patients with OSCC, and on an extensive public data (457) from TCGA database. Additionally, expression of TLK1 was significantly higher in OSCC tissues compared to that in adjacent normal tissues, which is negatively correlated with miR-16 expression in OSCC. Bioinformatics analyses exhibited that TLK1 is a potential downstream effector of miR-16 by directly targeting the 3'-untranslated regions (3'-UTR) of mRNA. Forced expression of miR-16 in OSCC cell lines inhibits cell proliferation in vitro, and tumor growth in vivo by inhibition of TLK1. Mechanistically, downregulation of TLK1 by miR-16 enhances higher level of DNA damage leading to a significant increase of G

Indexed as

3' Untranslated RegionsAnimalsCarcinoma, Squamous CellCell Line, TumorDisease ProgressionDNA DamageDown-RegulationFemaleG2 Phase Cell Cycle CheckpointsHumansKaplan-Meier EstimateMaleMiceMice, NudeMicroRNAsMiddle Aged3' Untranslated RegionsMicroRNAsMIRN16 microRNA, humanProtein Serine-Threonine KinasesTLK1 protein, humanDNA damagemiR-16Oral squamous cell carcinoma

Identifiers

PMID30252587
PMCPMC6226226
OpenAlexW2892954023

What OpenQuestion holds

Textmetadata
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.