Evidence map›Paper›PMID 26527623›Full record

ArticleMolecular & cellular proteomics : MCP2016

Translating Proteomic Into Functional Data: An High Mobility Group A1 (HMGA1) Proteomic Signature Has Prognostic Value in Breast Cancer.

Elisa Maurizio, Jacek R Wiśniewski, Yari Ciani, Angela Amato, Laura Arnoldo, Carlotta Penzo, Silvia Pegoraro, Vincenzo Giancotti, Alberto Zambelli, Silvano Piazza and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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 4 institutions in 2 countries.

Elisa MaurizioFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy;
Jacek R Wiśniewski§Biochemical Proteomics Group, Department of Proteomics and Signal Transduction, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany;
Yari Ciani¶Laboratorio Nazionale CIB, (LNCIB), Area Science Park, 34149 Trieste, Italy;
Angela Amato¶¶Laboratory of Experimental Oncology and Pharmacogenomics IRCCS - Salvatore Maugeri Foundation, 27100 Pavia, Italy;
Laura ArnoldoFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy;
Carlotta PenzoFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy;
Silvia PegoraroFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy;
Vincenzo GiancottiFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy;
Alberto Zambelli‖Department of Medical Oncology, Hospital Papa Giovanni XXIII, 24127 Bergamo, Italy.
Silvano Piazza¶Laboratorio Nazionale CIB, (LNCIB), Area Science Park, 34149 Trieste, Italy;
Guidalberto ManfiolettiFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy; rsgarra@units.it manfiole@units.it.
Riccardo SgarraFrom the ‡Department of Life Sciences, University of Trieste, 34127 Trieste, Italy; rsgarra@units.it manfiole@units.it.
University of Trieste · ITFondazione Salvatore Maugeri · ITMax Planck Institute of Biochemistry · DEOspedale Papa Giovanni XXIII · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is a very heterogeneous disease, and biological variability adds a further level of complexity, thus limiting the ability to identify new genes involved in cancer development. Oncogenes whose expression levels control cell aggressiveness are very useful for developing cellular models that permit differential expression screenings in isogenic contexts. HMGA1 protein has this unique property because it is a master regulator in breast cancer cells that control the transition from a nontumorigenic epithelial-like phenotype toward a highly aggressive mesenchymal-like one. The proteins extracted from HMGA1-silenced and control MDA-MB-231 cells were analyzed using label-free shotgun mass spectrometry. The differentially expressed proteins were cross-referenced with DNA microarray data obtained using the same cellular model and the overlapping genes were filtered for factors linked to poor prognosis in breast cancer gene expression meta-data sets, resulting in an HMGA1 protein signature composed of 21 members (HRS, HMGA1 reduced signature). This signature had a prognostic value (overall survival, relapse-free survival, and distant metastasis-free survival) in breast cancer. qRT-PCR, Western blot, and immunohistochemistry analyses validated the link of three members of this signature (KIFC1, LRRC59, and TRIP13) with HMGA1 expression levels both in vitro and in vivo and wound healing assays demonstrated that these three proteins are involved in modulating tumor cell motility. Combining proteomic and genomic data with the aid of bioinformatic tools, our results highlight the potential involvement in neoplastic transformation of a restricted list of factors with an as-yet-unexplored role in cancer. These factors are druggable targets that could be exploited for the development of new, targeted therapeutic approaches in triple-negative breast cancer.

Indexed as

ATPases Associated with Diverse Cellular ActivitiesBlotting, WesternBreast NeoplasmsCarrier ProteinsCell Cycle ProteinsCell Line, TumorDisease-Free SurvivalGene Expression Regulation, NeoplasticHMGA1a ProteinHumansImmunohistochemistryKaplan-Meier EstimateKinesinsMass SpectrometryMembrane ProteinsMultivariate AnalysisATPases Associated with Diverse Cellular ActivitiesCarrier ProteinsCell Cycle ProteinsHMGA1a ProteinKIFC1 protein, humanKinesinsLRRC59 protein, humanMembrane ProteinsProteomeTRIP13 protein, human

Identifiers

PMID26527623
PMCPMC4762532
OpenAlexW2263131704

What OpenQuestion holds

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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.