Evidence map›Paper›PMID 23785426›Full record

ArticlePloS one2013

Analysis and prediction of pathways in HeLa cells by integrating biological levels of organization with systems-biology approaches.

Juan Carlos Higareda-Almaraz, Ilse A Valtierra-Gutiérrez, Magdalena Hernandez-Ortiz, Sandra Contreras, Erika Hernandez, Sergio Encarnación-Guevara, Sergio Encarnacion

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. microPublication biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

  • Erratum issued
    Encarnacion, Sergio [corrected to Encarnación-Guevara, Sergio]
5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Juan Carlos Higareda-AlmarazFunctional Genomics of Prokaryotes Research Program, Center for Genomic Sciences, National Autonomous University of Mexico, Cuernavaca, Morelos, Mexico.
Ilse A Valtierra-Gutiérrez
Magdalena Hernandez-Ortiz
Sandra Contreras
Erika Hernandez
Sergio Encarnación-Guevara
Sergio Encarnacion
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has recently begun to be considered that cancer is a systemic disease and that it must be studied at every level of complexity using many of the currently available approaches, including high-throughput technologies and bioinformatics. To achieve such understanding in cervical cancer, we collected information on gene, protein and phosphoprotein expression of the HeLa cell line and performed a comprehensive analysis of the different signaling pathways, transcription networks and metabolic events in which they participate. A total expression analysis by RNA-Seq of the HeLa cell line showed that 19,974 genes were transcribed. Of these, 3,360 were over-expressed, and 2,129 under-expressed when compared to the NHEK cell line. A protein-protein interaction network was derived from the over-expressed genes and used to identify central elements and, together with the analysis of over-represented transcription factor motifs, to predict active signaling and regulatory pathways. This was further validated by Metal-Oxide Affinity Chromatography (MOAC) and Tandem Mass Spectrometry (MS/MS) assays which retrieved phosphorylated proteins. The 14-3-3 family members emerge as important regulators in carcinogenesis and as possible clinical targets. We observed that the different over- and under-regulated pathways in cervical cancer could be interrelated through elements that participate in crosstalks, therefore belong to what we term "meta-pathways". Additionally, we highlighted the relations of each one of the differentially represented pathways to one or more of the ten hallmarks of cancer. These features could be maintained in many other types of cancer, regardless of mutations or genomic rearrangements, and favor their robustness, adaptations and the evasion of tissue control. Probably, this could explain why cancer cells are not eliminated by selective pressure and why therapy trials directed against molecular targets are not as effective as expected.

Indexed as

Gene Expression ProfilingGene Regulatory NetworksHeLa CellsHumansSystems Biology

Identifiers

PMID23785426
PMCPMC3680226
OpenAlexW2075561913

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.