Examination of HMGA2 binding genes in human HMGA2-exogenous overexpressed gastric cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE174442 | GEO | 2021/08/18
REPOSITORIES: GEO
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Project description:Examination of HMGA2 binding genes in human HMGA2-exogenous overexpressed gastric cancer cells
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Project description:Although HMGA2 overexpression (OE) has been reported in several myeloid malignancies, its role in MDS remains unclear. To determine the role of HMGA2 in MDS pathogenesis, we generated MDS mice using patient-derived RUNX1 mutant, and overexpressed HMGA2 in this model. HMGA2-OE MDS mice developed non-infectious pneumonia. Prominent infiltration of neutrophils was observed in the lung tissue. RNA sequencing of HSC/Ps and neutrophils revealed that genes related to platelet activation are significantly activated in HMGA2-OE MDS mice. Flow cytometric analysis showed that P-selectin+ activated platelets tightly interact with neutrophils in the HMGA2-OE MDS mice. Genetic inhibition of P-selectin attenuated neutrophil activation and pneumonia development in the MDS mice. These findings provide new insights into mechanistic basis of systemic complications of MDS.
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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.
2011-02-06 | GSE24071 | GEO
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.
2011-02-06 | E-GEOD-24071 | biostudies-arrayexpress
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
2014-03-07 | E-GEOD-55340 | biostudies-arrayexpress
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
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.
2014-03-07 | GSE55340 | GEO
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.
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Project description:Congenital Heart Disease (CHD) is the most common birth defect and leading cause of infant mortality, yet molecular mechanisms explaining CHD remain mostly unknown. Sequencing studies are identifying CHD candidate genes at a brisk rate including MINK1, a serine/threonine kinase. However, a plausible molecular mechanism connecting CHD and MINK1 is unknown. Here, we reveal that mink1 is required for proper heart development due to its role in left right patterning. mink1 defines the cell fates of the Left-Right Organizer (LRO), a ciliated structure in the posterior mesoderm that breaks bilateral symmetry in vertebrate embryos. To identify mink1 targets, we applied an unbiased proteomics approach and identified the transcription factor, HMGA2. HMGA2 is necessary and sufficient for specifying Spemann’s Organizer, which can neuralize the ectoderm and dorsalize the mesoderm. Indeed, we demonstrate that HMGA2 is downstream of catenin, a critical effector of the Wnt signaling pathway that is well known to induce Spemann Organizer cell fates. In summary, we discover a transcription factor, HMGA2, that is downstream of mink1 that is critical for the specification of Spemann’s Organizer as well as the LRO defining a plausible mechanism for CHD.
2024-05-22 | PXD028827 | Pride
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.
2014-06-01 | GSE43739 | GEO