Evidence map›Paper›PMID 22736948›Full record

ArticleMolecular vision2012

YC-1 targeting of hypoxia-inducible factor-1α reduces RGC-5 cell viability and inhibits cell proliferation.

Leo Tsui, Tsorng-Harn Fong, I-Jong Wang

Abstract read
In one paragraph

Article in Molecular vision, 2012. 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
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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.

  1. Article
  2. Article
  3. [G protein-coupled receptor 17 is involved in CoClZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. On authentication of cell lines.Molecular vision · 2013
    Article
  8. 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

3 authors.

Leo TsuiGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Tsorng-Harn Fong
I-Jong Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe survival of retinal ganglion cells (RGCs) is a hallmark of many optic neurodegenerative diseases such as glaucoma. YC-1, a potential anticancer drug, is known to be able to decrease the stability and protein expression of hypoxia-inducible factor (HIF)-1α that is triggered by hypoxia and related to RGC survival. We hypothesized that YC-1 may alter RGC cell viability through the down-regulation of HIF-1α.

methodsCell viability of the RGC-5 cell line was measured with a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry, a LIVE/DEAD viability assay, and high-content screening (HCS) with MKI67 (K(i)-67) monoclonal antibodies were used to detect cell death and cellular proliferation.

resultsWe found that cells treated with 20 µM YC-1 for 24 h decreased the HIF-1α level in an RGC-5 cell line using immunoblotting and reduced the live cell number in an MTT assay. Results of flow cytometry and HCS demonstrated that reducing the cell proliferation of RGC-5 cells, not cell death, led to the decreased level in the MTT assay.

conclusionsOur findings demonstrate that YC-1-induced down-regulation of HIF-1α might reduce RGC cell proliferation and viability under normoxia, which implies a role of YC-1 in the neuroprotective effect for further clinical applications.

Indexed as

AntibodiesAntineoplastic AgentsApoptosisCell LineCell ProliferationCell SurvivalDose-Response Relationship, DrugDown-RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitIndazolesKi-67 AntigenRetinal Ganglion CellsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal Transduction3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazoleAntibodiesAntineoplastic AgentsHypoxia-Inducible Factor 1, alpha SubunitIndazolesKi-67 AntigenRNA, Messenger

Identifiers

PMID22736948
PMCPMC3380911

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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.