HMGA2

Last update 08 May 2025

Basic Info

Synonyms

BABL, high mobility group AT-hook 2, High mobility group AT-hook protein 2

+ [4]

Introduction

Functions as a transcriptional regulator. Functions in cell cycle regulation through CCNA2. Plays an important role in chromosome condensation during the meiotic G2/M transition of spermatocytes. Plays a role in postnatal myogenesis, is involved in satellite cell activation (By similarity). Positively regulates IGF2 expression through PLAG1 and in a PLAG1-independent manner (PubMed:28796236).

100 Clinical Results associated with HMGA2

100 Translational Medicine associated with HMGA2

0 Patents (Medical) associated with HMGA2

1,844

Literatures (Medical) associated with HMGA2

01 Jun 2025·Biochemistry and Biophysics Reports

Elevated expression of microRNA-155, microRNA-383, and microRNA-9 in Iranian patients with polycystic ovary syndrome

Article

Author: Roshanaei, Kambiz ; Afkhami, Hamed ; Heidarieh, Nasrin ; Faraji, Maryam

Background and objectivePolycystic ovary syndrome (PCOS) is a complex endocrine disorder with both genetic and environmental components. Recent studies have highlighted the potential role of microRNAs (miRNAs) and single nucleotide polymorphisms (SNPs) in its pathogenesis. This study aimed to investigate the association of three SNPs (rs2252673, rs2272046, and rs1894116) in the INSR, HMGA2, and YAP1 genes, respectively, with PCOS, as well as the expression levels of miR-155, miR-383, and miR-9 in Iranian patients.MethodsWe included 100 PCOS patients and 100 healthy controls. DNA and RNA were extracted from blood samples. SNP genotyping was performed using tetra-primer ARMS-PCR, while miRNA expression levels were quantified using quantitative reverse transcription PCR (qRT-PCR). Logistic regression and ANOVA tests were used for statistical analysis, and Pearson's correlation test (PcT) was applied to assess relationships between miRNA expression profiles.ResultsNo significant associations were observed between the investigated SNPs (rs2252673, rs2272046, and rs1894116) and PCOS risk. However, logistic regression analysis revealed a significant difference for rs1894116 under dominant (P = 0.045) and recessive (P = 0.001) models. Notably, the expression levels of miR-155, miR-383, and miR-9 were significantly upregulated in PCOS patients compared to controls, with fold changes of 13.5, 4.13, and 10.7, respectively (P < 0.05).LimitationsThis study has several limitations, including the relatively small sample size (n = 100 per group) and the ethnic-specific nature of the population studied, which may limit generalizability to other populations.ConclusionOur findings suggest that miR-155, miR-383, and miR-9 are significantly upregulated in Iranian PCOS patients, highlighting their potential as biomarkers or therapeutic targets. However, no significant associations were found between the investigated SNPs and PCOS risk. Future studies with larger, multi-ethnic cohorts are warranted to validate these findings and explore the molecular mechanisms underlying the roles of these miRNAs in PCOS pathophysiology.

01 May 2025·European Journal of Pharmacology

Inhibition of ULK1 attenuates ferroptosis-mediated cardiac hypertrophy via HMGA2/METTL14/SLC7A11 axis in mice

Article

Author: Shi, Pilong ; Liu, Yongsheng ; Jiang, Man ; Liu, Yuhang ; Ba, Lina ; Sha, Yuetong ; Cao, Yonggang ; Wang, Jiaxin ; Zhang, Meitian ; Qi, Hanping ; Zhang, Qianhui ; Sun, Hongli

UNC-51-like kinase 1 (ULK1), a primary serine/threonine kinase, is implicated in diverse pathophysiological processes. Previous findings have linked ULK1-dependent autophagy to cardiac hypertrophy. Our study further explored the functional role and molecular mechanisms of ULK1 in non-autophagic signaling pathways. Notably, ULK1 expression was significantly elevated in both transverse aortic constriction (TAC)-induced hypertrophic mouse hearts and Angiotensin II (Ang II)-treated cardiomyocytes, suggesting an increased sensitivity to hypertrophic stimuli potentially mediated by ULK1-induced ferroptosis in hypertrophic cardiomyocytes. Treatment with the ferroptosis inhibitor ferrostatin-1 (Fer-1) effectively reduced ULK1-induced cardiomyocyte hypertrophy and ferroptosis. Proteomic analysis identified the upregulation of transcription factor high mobility group A2 (HMGA2) as a key mechanism in this ferroptotic process. Elevated HMGA2 levels exacerbated ferroptosis, evidenced by increased cell death, lipid peroxidation, ROS production, and reduced GPX4 expression. Furthermore, HMGA2 was shown to promote cardiomyocyte ferroptosis via binding to methyltransferase-like 14 (METTL14), which in turn enhanced ferroptosis in cardiomyocytes through solute carrier family 7 member 11 (SLC7A11) m⁶A modification. In vivo, a delivery system using neutrophil membrane (NM)-coated mesoporous silica nanoparticles (MSN) was developed to inhibit cardiac hypertrophy, underscoring the therapeutic potential of targeting ULK1. Overall, this study demonstrates that ULK1 promotes cardiac hypertrophy through HMGA2/METTL14/SLC7A11 axis-mediated cardiomyocyte ferroptosis, suggesting a novel therapeutic approach for cardiac hypertrophy.

02 Apr 2025·Environmental Epigenetics

Non-genotoxic carcinogens (TPA and mezerein) activate tumourous transformation through miR let-7-mediated Hmga2 expression in Bhas42 cells

Article

Author: Kim, Minjeong ; Min, Euijun ; Park, Heejin ; Jang, Sumi ; Lee, Byoung-Seok ; Kim, Younhee ; Hyun, Sung-Ae ; Ko, Moon Yi ; Ka, Minhan

AbstractA Bhas42 cell transformation assay is a method used to detect the tumour-promoting activities of chemicals. However, the mechanisms underlying tumour transformations mediated by non-genotoxic carcinogens (NGCs) are poorly understood. This study aimed to examine the correlation between 12-O-tetradecanoylphorbol 13-acetate (TPA) or mezerein and the initiation of tumourous transformations by epigenetic regulation in Bhas42 cells. We found that TPA and mezerein prompted tumourous transformations by stimulating cell proliferation and migration in Bhas42 cells. Furthermore, we observed alterations in the expression levels of 134 genes, with 87 genes being upregulated and 47 genes being downregulated, following exposure to either TPA or mezerein. Among the differentially regulated genes, we identified 17 upregulated genes and 8 downregulated genes corresponding to differentially expressed genes in TNM [primary tumour (T), regional nodes (N), and metastasis (M)]. Importantly, we found that TPA and mezerein triggered the expression of Hmga2 and Ezh2 by loss of miRNA let-7 (miR let-7) in Bhas42 cells. Finally, the microRNA (miRNA) mimic of let-7 prevented the TPA- and mezerein-induced activation of Hmga2 and Ezh2 in Bhas42 cells. Our findings reveal a connection between tumourous transformations and the epigenetic regulator miR let-7 in NGCs, such as TPA and mezerein in Bhas42 cells. This highlights miR let-7 as a promising therapeutic target for mitigating tumourous transformations induced by NGCs.

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HMGA2

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