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HMGA2/TET1/HOXA9 pathway regulates breast cancer growth and metastasis.

ABSTRACT: HMGA2, Tet1 and HOXA9 are all regulated human breast tumorigenesis. We use gene expression array analysis to identify and compare the genes regulated by HMGA2, Tet1 and/or HOXA9 in human breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43741 | GEO | 2013/06/03

SECONDARY ACCESSION(S): PRJNA187192

REPOSITORIES: GEO

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HMGA2/TET1/HOXA9 pathway regulates breast cancer growth and metastasis

Project description: Not available

| S-ECPF-GEOD-43741 | biostudies-other

HMGA2/TET1/HOXA9 signaling pathway regulates breast cancer growth and metastasis.

Project description: Not available

| S-EPMC3683728 | biostudies-literature

HMGA2/TET1/HOXA9 pathway regulates breast cancer growth and metastasis.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-03 | E-GEOD-43741 | biostudies-arrayexpress

Homo sapiens

Project description:HMGA2/TET1/HOXA9 pathway regulates breast cancer growth and metastasis.

| PRJNA187192 | ENA

MicroRNA expression array of 1833 cells: control vs. HMGA2 shRNA

Project description:HMGA2 has been implicated in tumor progression. Identification of microRNAs regulated by HMGA2 helps us to understand how HMGA2 regulates tumor metastasis via its downstream target mircoRNAs and genes. Total RNA was extracted from 1833 cells with control or depleted HMGA2 expression, respectively. Exiqon miRCURY LNA 5th generation expression array was performed to identify the microRNAs regulated by HMGA2.

2014-06-01 | E-GEOD-43739 | biostudies-arrayexpress

HMGA2 overexpression

Project description:Overexpression of high mobility group AT-hook 2 (HMGA2) associated with truncations of its 3’ untranslated region (UTR) with let-7 micro RNA-complementary sequences have been identified in patients with paroxysmal nocturnal hemoglobinuria (PNH). Here, we generated transgenic mice (∆Hmga2 mice) with a 3’UTR-trncated Hmga2 cDNA that overexpress Hmga2 mRNA and protein in hematopoietic organs. ∆Hmga2 mice showed proliferative hematopoiesis that mimicked a myeloproliferative neoplasm (MPN)-like phenotype with increased numbers of all lineages of peripheral blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis, and erythropoietin-independent erythroid colony formation compared to wild-type mice. ∆Hmga2 BM-derived cells took over most of hematopoiesis in competitive repopulations during serial BM transplants. When we bred mice with circulating PNH cells (Piga- mice) with ∆Hmga2 mice, the lack of GPI-linked proteins did not add an additional clonal advantage to the ∆Hmga2+ cells. In summary, our results showed that the overexpression of a 3’UTR-truncated Hmga2 leads to a proliferative hematopoiesis with clonal advantage, which may explain clonal expansion in PNH or MPN at the level of HSC.

2011-02-06 | GSE24071 | GEO

MicroRNA expression array of 1833 cells: control vs. HMGA2 shRNA

2014-06-01 | GSE43739 | GEO

HMGA2 overexpression

2011-02-06 | E-GEOD-24071 | biostudies-arrayexpress

HMGA2 regulates ATF4 and the serine biosynthesis genes and reprograms metabolism in breast cancer

Project description:The transcription regulator High Mobility Group AT-Hook 2 (HMGA2) plays an important role in many types of cancers, but the molecular mechanisms are not fully elucidated. We found by knock-down studies that HMGA2 controls expression of ATF4 and the enzymes in the serine synthesis pathway in triple negative breast cancer cells, and that HMGA2 expression correlates with poor clinical outcome in ER negative breast cancers. Furthermore, we found that the metabolism was dysregulated in cells with reduced HMGA2 expression, which affected their response to mitochondrial stressors and to changed carbon sources. Altogether, our findings demonstrate that HMGA2 is a regulator of serine biosynthesis and metabolism, consistent with the well-known role of HMGA2 as a regulator of proliferation, epithelial-mesenchymal transition and stemness.

2019-12-31 | GSE118857 | GEO

Examination of HMGA2 binding genes in human HMGA2-exogenous overexpressed gastric cancer cells

Project description:HMGA2 significantly increased cell proliferation capacity of gastric cancer in a HMGA2-dependent manner both in vivo and in vitro and we found HMGA2 promoted GC through accelerating S-G2/M phase.To elucidate the underlining mechanism by which HMGA2 induced the change of phenotype in GC cells, we performed ChIP-seq analysis of HMGA2-OE MKN-45 cells with anti-HMGA2 antibody.

2021-08-18 | GSE174442 | GEO

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