ArticleInternational journal of molecular medicine2019
HMGA2 regulates acute myeloid leukemia progression and sensitivity to daunorubicin via Wnt/β-catenin signaling.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- HMGA2 overexpression with specific chromosomal abnormalities predominate in CALR and ASXL1 mutated myelofibrosis.Leukemia · 2025Article
- Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025Review
- Auto-expansion ofMolecular therapy. Methods & clinical development · 2024Article
- Silencing LINC00987 ameliorates adriamycin resistance of acute myeloid leukemia via miR-4458/HMGA2 axis.Biology direct · 2024Article
- Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mink1 regulates spemann organizer cell fate in the xenopus gastrula via Hmga2.Developmental biology · 2023Article
- Amentoflavone inhibits colorectal cancer epithelial-mesenchymal transition via the miR-16-5p/Annals of translational medicine · 2022Article
- Lin28a induces SOX9 and chondrocyte reprogramming via HMGA2 and blunts cartilage loss in mice.Science advances · 2022Article
- Exosomal microRNA-107 reverses chemotherapeutic drug resistance of gastric cancer cells through HMGA2/mTOR/P-gp pathway.BMC cancer · 2021Article
- Regulatory effect between HMGA2 and the Wnt/β-catenin signaling pathway in the carcinogenesis of sporadic colorectal tubular adenoma.Oncology letters · 2021Article
- Silencing of circTASP1 inhibits proliferation and induces apoptosis of acute myeloid leukaemia cells through modulating miR-515-5p/HMGA2 axis.Journal of cellular and molecular medicine · 2021Article
- Therapeutic Targeting of the Leukaemia Microenvironment.International journal of molecular sciences · 2021Review
- HMGA Proteins in Hematological Malignancies.Cancers · 2020Review
- A-kinase interacting protein 1 might serve as a novel biomarker for worse prognosis through the interaction of chemokine (C-X-C motif) ligand 1/chemokine (C-X-C motif) ligand 2 in acute myeloid leukemia.Journal of clinical laboratory analysis · 2020Article
- CircRNAs as New Therapeutic Entities and Tools for Target Identification in Acute Myeloid Leukemia.Cancer genomics & proteomicsReview
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a malignant disease with an increasing prevalence in adults and children. However, valuable molecular diagnostic research is rare. In the present study, plasmids silencing and overexpressing high‑mobility group AT‑hook 2 (HMGA2) were respectively transfected in HL60 and NB4 cells. The effects of HMGA2 on AML cell viability, apoptosis, migration and invasion were determined by preforming MTT, flow cytometry, wound scratch and Transwell assays, respectively. Genes associated with apoptosis and Wnt signaling were evaluated by reverse transcription‑quantitative (RT‑q)‑PCR and western blotting. AML cell sensitivity to daunorubicin (DNR) and the regulatory effects of the Wnt signaling pathway via HMGA2 following treatment with the agonist LiCl or antagonist XAV939 were detected by MTT, RT‑qPCR and western blot analysis. The results revealed that the expression of HMGA2 was elevated more so in HL60, KG1, U937, Kasumi‑1, THP‑1 and K562 cells than in NB4 cells. Silencing HMGA2 suppressed cell viability, migration and invasion, enhanced cell apoptosis and sensitivity to DNR, and almost restored the DNR inhibitory function that was promoted by LiCl treatment. In addition, low expression of HMGA2 attenuated X‑linked inhibitor of apoptosis and Bcl‑2 mRNA and protein levels, and upregulated the expression of Bax and cleaved‑caspase‑3. Furthermore, silencing HMGA2 not only decreased Wnt and non‑phospho‑β‑catenin expressions, but also partially reversed the increased expressions of these proteins induced by LiCl treatment. On the other hand, overexpression of HMGA2 exhibited the opposite results after transfection in NB4 cells. The results of the present study demonstrated that HMGA2 played important roles in driving AML progression and chemosensitivity in HL60 and NB4 cells, potentially by activating the Wnt/β‑catenin signaling pathway. Therefore, it was suggested that HMGA2 may be a promising molecular marker for AML diagnosis.
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