ArticleMolecular and cellular biochemistry2011
High-mobility group A1 proteins enhance the expression of the oncogenic miR-222 in lung cancer cells.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 47 citations in OpenAlex.
- Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.Cancer cell international · 2025Review
- Review
- Non-coding RNA transcripts, incredible modulators of cisplatin chemo-resistance in bladder cancer through operating a broad spectrum of cellular processes and signaling mechanism.Non-coding RNA research · 2024Review
- MicroRNAs as the critical regulators of autophagy-mediated cisplatin response in tumor cells.Cancer cell international · 2023Review
- Deciphering the Role of microRNA Mediated Regulation of Coronin 1C in Glioblastoma Development and Metastasis.Non-coding RNA · 2023Article
- HMGA1 gene expression level in cancer tissue and blood samples of non-small cell lung cancer (NSCLC) patients: preliminary report.Molecular genetics and genomics : MGG · 2022Article
- High Mobility Group A 1 Expression as a Poor Prognostic Marker Associated with Tumor Invasiveness in Gastric Cancer.Life (Basel, Switzerland) · 2022Article
- HMGA1 positively regulates the microtubule-destabilizing protein stathmin promoting motility in TNBC cells and decreasing tumour sensitivity to paclitaxel.Cell death & disease · 2022Article
- HMGA1 promotes gastric cancer growth and metastasis by transactivating SUZ12 and CCDC43 expression.Aging · 2021Article
- Emerging roles and mechanisms of microRNA‑222‑3p in human cancer (Review).International journal of oncology · 2021Review
- High-mobility group AT-hook 1 promotes cardiac dysfunction in diabetic cardiomyopathy via autophagy inhibition.Cell death & disease · 2020Article
- Downregulation of HMGA1 Mediates Autophagy and Inhibits Migration and Invasion in Bladder Cancer via miRNA-221/TP53INP1/p-ERK Axis.Frontiers in oncology · 2020Article
- HMGA1 in cancer: Cancer classification by location.Journal of cellular and molecular medicine · 2019Review
- Inhibition of Triple-Negative Breast Cancer Cell Aggressiveness by Cathepsin D Blockage: Role of Annexin A1.International journal of molecular sciences · 2019Article
- Role of miR-221/222 in Tumor Development and the Underlying Mechanism.Journal of oncology · 2019Article
- HMGA1 exacerbates tumor growth through regulating the cell cycle and accelerates migration/invasion via targeting miR-221/222 in cervical cancer.Cell death & disease · 2018Article
- Upregulation of miR-614 promotes proliferation and inhibits apoptosis in ovarian cancer by suppressing PPP2R2A expression.Molecular medicine reports · 2018Article
- Profiling of 179 miRNA Expression in Blood Plasma of Lung Cancer Patients and Cancer-Free Individuals.Scientific reports · 2018Article
- Dynamic and Modularized MicroRNA Regulation and Its Implication in Human Cancers.Scientific reports · 2017Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group A1 (HMGA1) is a non-histone chromatin protein that has the ability to regulate the transcriptional activity of many genes. Overexpression of HMGA1 is associated with malignant cellular behavior in a range of human cancers but the underlying mechanism is largely unknown. Here we showed that in a cohort of non-small cell lung cancer (NSCLC) tumors, HMGA1 overexpression was immediately associated with enhanced expression of an oncogenic miRNA, namely, miR-222. Chromatin immunoprecipitation (CHIP) assay revealed that HMGA1 directly binds to the proximal promoter of miR-222 in NSCLC cells. We further showed that HMGA1 silencing reduced miR-222 transcriptional activity, whereas forced HMGA1 expression increased it, indicating that miR-222 is directly regulated by HMGA1. Based on in silico prediction, one of the putative targets of miR-222 is phosphatase 2A subunit B (PPP2R2A) which inhibits Akt phosphorylation (p-Akt). We demonstrated that miR-222 inhibited protein expression of PPP2R2A in NSCLC cells by directly interacting with its 3'-UTR region, leading to an obvious increase of p-Akt. HMGA1 silencing augmented PPP2R2A protein expression and inhibited Akt signaling, resulting in significantly retarded cell growth response to IGF-I. These results suggested that HMGA1 is a positive regulator of miR-222, and HMGA1 overexpression might contribute to dysregulation of Akt signaling in NSCLC.
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