Evidence map›Paper›PMID 20576167›Full record

ArticleBMC cancer2010

Identification of target genes for wild type and truncated HMGA2 in mesenchymal stem-like cells.

Jørn Henriksen, Marianne Stabell, Leonardo A Meza-Zepeda, Silje Au Lauvrak, Moustapha Kassem, Ola Myklebost

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. 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
1.2field-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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. AI/ML-Assisted Detection ofInternational journal of molecular sciences · 2025
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  12. Article
  13. High mobility group A2 (HMGA2) promotes EMT via MAPK pathway in prostate cancer.Biochemical and biophysical research communications · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. HMGA2 and high-grade serous ovarian carcinoma.Journal of molecular medicine (Berlin, Germany) · 2013
    Review
  18. 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

6 authors at 4 institutions in 2 countries.

Jørn HenriksenCAST, Cancer Stem Cell Innovation Centre, Department of Tumor Biology, The Norwegian Radium Hospital, Oslo University Hospital, N-0027 Oslo, Norway.
Marianne Stabell
Leonardo A Meza-Zepeda
Silje Au Lauvrak
Moustapha Kassem
Ola Myklebost
Oslo University Hospital · NOKing Saud University · SANorwegian Cancer Society · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe HMGA2 gene, coding for an architectural transcription factor involved in mesenchymal embryogenesis, is frequently deranged by translocation and/or amplification in mesenchymal tumours, generally leading to over-expression of shortened transcripts and a truncated protein.

methodsTo identify pathways that are affected by sarcoma-associated variants of HMGA2, we have over-expressed wild type and truncated HMGA2 protein in an immortalized mesenchymal stem-like cell (MSC) line, and investigated the localisation of these proteins and their effects on differentiation and gene expression patterns.

resultsOver-expression of both transgenes blocked adipogenic differentiation of these cells, and microarray analysis revealed clear changes in gene expression patterns, more pronounced for the truncated protein. Most of the genes that showed altered expression in the HMGA2-overexpressing cells fell into the group of NF-kappaB-target genes, suggesting a central role for HMGA2 in this pathway. Of particular interest was the pronounced up-regulation of SSX1, already implicated in mesenchymal oncogenesis and stem cell functions, only in cells expressing the truncated protein. Furthermore, over-expression of both HMGA2 forms was associated with a strong repression of the epithelial marker CD24, consistent with the reported low level of CD24 in cancer stem cells.

conclusionsWe conclude that the c-terminal part of HMGA2 has important functions at least in mesenchymal cells, and the changes in gene expression resulting from overexpressing a protein lacking this domain may add to the malignant potential of sarcomas.

Indexed as

Gene Expression ProfilingGene Expression Regulation, NeoplasticAdipocytesBiomarkersBlotting, NorthernBlotting, WesternCell DifferentiationCell LineageCells, CulturedFlow CytometryHMGA2 ProteinHumansMesenchymal Stem CellsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionBiomarkersHMGA2 ProteinRNA, Messenger

Identifiers

PMID20576167
PMCPMC2912264
OpenAlexW2152566924

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Registered trials

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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.