Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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


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) by reprogramming cancer cells to a stem-like state. We 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. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.

ORGANISM(S): Homo sapiens

SUBMITTER: Linda Resar 

PROVIDER: E-GEOD-45483 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Shah Sandeep N SN   Cope Leslie L   Poh Weijie W   Belton Amy A   Roy Sujayita S   Talbot C Conover CC   Sukumar Saraswati S   Huso David L DL   Resar Linda M S LM  

PloS one 20130502 5


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 grow  ...[more]

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