Evidence map›Paper›PMID 23658826›Full record

ArticlePloS one2013

HMGA1: a master regulator of tumor progression in triple-negative breast cancer cells.

Sandeep N Shah, Leslie Cope, Weijie Poh, Amy Belton, Sujayita Roy, C Conover Talbot, Saraswati Sukumar, David L Huso, Linda M S Resar

Open 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. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  6. Spiegelmer Aptamers: Innovative Approach in Breast Cancer.Breast cancer : basic and clinical research · 2026
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23 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Sandeep N ShahHematology Division, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Leslie Cope
Weijie Poh
Amy Belton
Sujayita Roy
C Conover Talbot
Saraswati Sukumar
David L Huso
Linda M S Resar
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Mechanisms of Neoplastic Transformation by HMG-I/YR01CA092339 · NCI · JOHNS HOPKINS UNIVERSITY · PI RESAR, LINDA M S · 2003 to 2006
$1.2M
NCI NIH HHS R01 CA092339NCI NIH HHS R21 CA2149550-0131
6 · The paper itself

Abstract

Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231, Hs578T) by reprogramming cancer cells to a stem-like state. Silencing HMGA1 expression in invasive, aggressive breast cancer cells dramatically halts cell growth and results in striking morphologic changes from mesenchymal-like, spindle-shaped cells to cuboidal, epithelial-like cells. Mesenchymal genes (Vimentin, Snail) are repressed, while E-cadherin is induced in the knock-down cells. Silencing HMGA1 also blocks oncogenic properties, including proliferation, migration, invasion, and orthotopic tumorigenesis. Metastatic progression following mammary implantation is almost completely abrogated in the HMGA1 knock-down cells. Moreover, silencing HMGA1 inhibits the stem cell property of three-dimensional mammosphere formation, including primary, secondary, and tertiary spheres. In addition, knock-down of HMGA1 depletes cancer initiator/cancer stem cells and prevents tumorigenesis at limiting dilutions. We also discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy.

Indexed as

Disease ProgressionCarcinogenesisCell Line, TumorCell ProliferationGene Knockdown TechniquesGene SilencingHMGA1a ProteinHumansMesodermNeoplasm InvasivenessNeoplasm MetastasisNeoplastic Stem CellsTriple Negative Breast NeoplasmsHMGA1a Protein

Identifiers

PMID23658826
PMCPMC3642138
OpenAlexW2076131887

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.