Evidence map›Paper›PMID 26339371›Full record

ArticleInternational journal of clinical and experimental pathology2015

Mir-192 suppresses apoptosis and promotes proliferation in esophageal aquamous cell caicinoma by targeting Bim.

Shujun Li, Feng Li, Ren Niu, Helin Zhang, Airong Cui, Wenting An, Xiaolu Wang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. miR-192 Is Overexpressed and Promotes Cell Proliferation in Prostate Cancer.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2019
    Article
  9. Article
  10. Article
  11. Low miR-192 expression predicts poor prognosis in pediatric acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. microRNA regulators of apoptosis in cancer.Discoveries (Craiova, Romania) · 2016
    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

7 authors at 1 institution in 1 country.

Shujun LiDepartment of Thoracic Surgery, Second Hospital of Hebei Medical University Shijiazhuang, China.
Feng LiDepartment of Cancer Center, Second Hospital of Hebei Medical University Shijiazhuang, China.
Ren NiuDepartment of Cancer Center, Second Hospital of Hebei Medical University Shijiazhuang, China.
Helin ZhangDepartment of Thoracic Surgery, Second Hospital of Hebei Medical University Shijiazhuang, China.
Airong CuiDepartment of Pathology, Second Hospital of Hebei Medical University Shijiazhuang, China.
Wenting AnDepartment of Central Laboratory, Second Hospital of Hebei Medical University Shijiazhuang, China.
Xiaolu WangDepartment of Cancer Center, Second Hospital of Hebei Medical University Shijiazhuang, China.
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small, non-coding RNAs of endogenous origin. Accumulating studies have shown aberrant miRNA expression plays an important role in many tumor types. However, the mechanisms by which miRNAs regulate esophageal squamous cell carcinoma (ESCC) development remain poorly understood. In the present study, we assayed expression level of miR-192 in ESCC tissues and cell lines by real-time PCR, and defined the target gene and biological function by luciferase reporter assay, Western blot and apoptosis assay. We first verified that the expression level of miR-192 was significantly increased in ESCC tissues and cancer cells. Moreover, miR-192 over-expression inhibited cells apoptosis and promoted ESCC cells proliferation. We further demonstrated that miR-192 directly targeted 3'-UTR of Bim gene, and inhibited its protein expression. Importantly, Bim could reduce ESCC cells apoptosis ability induced by miR-192. These data suggest an important role of miR-192 in the molecular etiology of ESCC and implicate the potential application of miR-192 in ESCC therapy.

Indexed as

ApoptosisCell Proliferation3' Untranslated RegionsApoptosis Regulatory ProteinsBcl-2-Like Protein 11Binding SitesBlotting, WesternCarcinoma, Squamous CellCell Line, TumorEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticGenes, ReporterHumansMale3' Untranslated RegionsApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl-2-Like Protein 11Membrane ProteinsMicroRNAsMIRN192 microRNA, humanProto-Oncogene ProteinsapoptosisBimESCCmiR-192

Identifiers

PMID26339371
PMCPMC4555699
OpenAlexW1237978947

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.