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HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis

ABSTRACT: Triple-negative breast cancer (TNBC), the most lethal breast cancer subtype, demonstrates poor prognosis due to its high rates of metastasis, recurrence, and mortality. The metastatic potential in TNBC patients serves as a critical determinant of clinical outcomes. The high mobility group AT-hook 2 (HMGA2) has emerged as a novel chromatin architectural regulator, its specific role in TNBC metastasis requires further investigation.To investigate the mechanism of HMGA2 regulation of TNBC metastasis,we performed RNA-sequencing using shNC or shHMGA2 from MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE296619 | GEO | 2025/06/16

REPOSITORIES: GEO

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HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis

Project description:HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis

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Project description:We sought to identify critical factors regulating muscle stem cell activation and commitment, and determined through loss-of-function analyses that HMGA2 (high mobility group AT-hook 2) is a key regulator of myogenesis both in vitro and in vivo. mRNAs were isolated from Hmga2 -/- and Hmga2 +/+ mice myoblasts, and a microarray experiment was performed.

2012-12-01 | E-GEOD-41907 | 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.

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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. Eight independent preparations of RNA, which included each 2 samples of KLS cells and MEP cells from ∆Hmga2 mice and 2 each from WT mice. Each preparation was made from 4 or 6 mice.

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HMGA2 overexpression

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Hmga2 is required for canonical WNT signaling during lung development

Project description:The high-mobility-group (HMG) proteins are the most abundant non-histone chromatin-associated proteins. Here we deciphered the role of the high mobility group AT-hook protein 2 (HMGA2) during lung development by analyzing the lung of Hmga2 deficient mice (Hmga2-/-).We found that Hmga2 is expressed in the mouse embryonic lung at the distal airways. Analysis of Hmga2-/- mice showed that Hmga2 is required for proper cell proliferation and distal epithelium differentiation during embryonic lung development. Hmga2 knockout (KO) led to enhanced canonical WNT signaling due to an increased expression of secreted WNT glycoproteins Wnt2b, Wnt7b and Wnt11 as well as a reduction of the WNT signaling antagonizing proteins GATA6 (GATA binding protein 6) and FZD2 (frizzled homolog 2). Comparison of Hmga2-/- with Hmga2+/+ mice by Affymetrix microarray-based expression analysis of embryonic lung revealed an increased expression of genes whose products participate in cell cycle and canonical Wnt signaling. Affymetrix microarray transcriptome analysis of Hmga2-/- and Hmga2+/+ embryonic lung (E18.5) was performed and analyzed

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ROLE OF HMGA2 IN THE EPITHELIAL TO MESENCHYMAL TRANSITION ASSOCIATED WITH ENDOMETRIAL CARCINOGENESIS

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