Evidence map›Paper›PMID 23106301›Full record

ArticleCell proliferation2012

The mechanisms of nadroparin-mediated inhibition of proliferation of two human lung cancer cell lines.

Y Carmazzi, M Iorio, C Armani, S Cianchetti, F Raggi, T Neri, C Cordazzo, S Petrini, R Vanacore, F Bogazzi and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cytotoxicity of withasteroids: withametelin induces cell cycle arrest at G2/M phase and mitochondria-mediated apoptosis in non-small cell lung cancer A549 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  7. Review
  8. Article
  9. Significantly inhibitory effects of low molecular weight heparin (Fraxiparine) on the motility of lung cancer cells and its related mechanism.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  10. Article
  11. Rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke is dependent on Ca2+ mobilization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014
    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

12 authors at 3 institutions in 1 country.

Y CarmazziLaboratory of Respiratory Cell Biology, Cardiac, Thoracic and Vascular Department, University of Pisa and University Hospital of Pisa, Pisa, Italy.
M Iorio
C Armani
S Cianchetti
F Raggi
T Neri
C Cordazzo
S Petrini
R Vanacore
F Bogazzi
P Paggiaro
A Celi
Azienda Ospedaliera Universitaria Pisana · ITUniversity of Pisa · ITIstituto Nazionale per le Ricerche Cardiovascolari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesClinical data suggest that heparin treatment improves survival of lung cancer patients, but the mechanisms involved are not fully understood. We investigated whether low molecular weight heparin nadroparin, directly affects lung cancer cell population growth in conventionally cultured cell lines. MATERIALS AND

methodsA549 and CALU1 cells' viability was assessed by MTT and trypan blue exclusion assays. Cell proliferation was assessed using 5-bromo-2-deoxyuridine incorporation. Apoptosis and cell-cycle distribution were analysed by flow cytometry; cyclin B1, Cdk1, p-Cdk1 Cdc25C, p-Cdc25C and p21 expressions were analysed by western blotting. mRNA levels were analysed by real time RT-PCR.

resultsNadroparin inhibited cell proliferation by 30% in both cell lines; it affected the cell cycle in A549, but not in CALU-1 cells, inducing arrest in the G(2) /M phase. Nadroparin in A549 culture inhibited cyclin B1, Cdk1, Cdc25C and p-Cdc25C, while levels of p-Cdk1 were elevated; p21 expression was not altered. Dalteparin caused a similar reduction in A549 cell population growth; however, it did not alter cyclin B1 expression as expected, based on previous reports. Fondaparinux caused minimal inhibition of A549 cell population growth and no effect on either cell cycle or cyclin B1 expression.

conclusionsNadroparin inhibited proliferation of A549 cells by inducing G(2) /M phase cell-cycle arrest that was dependent on the Cdc25C pathway, whereas CALU-1 cell proliferation was halted by as yet not elucidated modes.

Indexed as

AdenocarcinomaAnticoagulantsApoptosisCarcinoma, Squamous Cellcdc25 PhosphatasesCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalFlow CytometryHumansLungLung NeoplasmsNadroparinAnticoagulantsCDC25C protein, humancdc25 PhosphatasesNadroparin

Identifiers

PMID23106301
PMCPMC6495835
OpenAlexW2063134389

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.