ArticleCancer science2007
High mobility group protein HMGA1 inhibits retinoblastoma protein-mediated cellular G0 arrest.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- miRNA expression changes during the course of neoadjuvant bevacizumab and chemotherapy treatment in breast cancer.Molecular oncology · 2019Trial
- HMGA1 regulates trabectedin sensitivity in advanced soft-tissue sarcoma (STS): A Spanish Group for Research on Sarcomas (GEIS) study.Cellular and molecular life sciences : CMLS · 2024Article
- HMGA1 Is a Potential Driver of Preeclampsia Pathogenesis by Interference with Extravillous Trophoblasts Invasion.Biomolecules · 2021Review
- Interplay between HMGA and TP53 in cell cycle control along tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- HMGA Genes and Proteins in Development and Evolution.International journal of molecular sciences · 2020Review
- Article
- HMGA1 promotes breast cancer angiogenesis supporting the stability, nuclear localization and transcriptional activity of FOXM1.Journal of experimental & clinical cancer research : CR · 2019Article
- HMGA1 in cancer: Cancer classification by location.Journal of cellular and molecular medicine · 2019Review
- Histone Citrullination Represses MicroRNA Expression, Resulting in Increased Oncogene mRNAs in Somatolactotrope Cells.Molecular and cellular biology · 2018Article
- 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
- A novel HMGA1-CCNE2-YAP axis regulates breast cancer aggressiveness.Oncotarget · 2015Article
- High mobility group A1 protein acts as a new target of Notch1 signaling and regulates cell proliferation in T leukemia cells.Molecular and cellular biochemistry · 2013Article
- Hmga1 is differentially expressed and mediates silencing of the CD4/CD8 loci in T cell lineages and leukemic cells.Cancer science · 2012Article
- HMGA1 drives stem cell, inflammatory pathway, and cell cycle progression genes during lymphoid tumorigenesis.BMC genomics · 2011Article
- pRb, a local chromatin organizer with global possibilities.Chromosoma · 2010Review
- HMGA1 is induced by Wnt/beta-catenin pathway and maintains cell proliferation in gastric cancer.The American journal of pathology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoblastoma protein (RB) acts as a tumor suppressor in many tissue types, by promoting cell arrest via E2F-mediated transcriptional repression. In addition to the aberrant forms of the RB gene found in different types of cancers, many viral oncoproteins including the simian virus 40 large T antigen target RB. However, cellular factors that inhibit RB function remain to be elucidated. Here, we report that RB interacts with the high mobility group protein A1 (HMGA1), a-non-histone architectural chromatin factor that is frequently overexpressed in cancer cells. HMGA1 binds the small pocket domain of RB, and competes with HDAC1. Subsequently, overexpression of HMGA1 abolishes the inhibitory effect of RB on E2F-activated transcription from the cyclin E promoter. Under serum starvation, T98G cells had been previously shown to be arrested in the G0 phase in an RB-mediated manner. The G0 phase was characterized by growth arrest and low levels of transcription, together with the hypophosphorylation of RB and the downregulation of HMGA1. In contrast, such serum-depleted G0 arrest was abrogated in T98G cells overexpressing HMGA1. The overexpressed HMGA1 was found to form complexes with cellular RB, suggesting that downregulation of HMGA1 is required for G0 arrest. There were no phenotypic changes in HMGA1-expressing T98G cells in the presence of serum, but the persistent expression of HMGA1 under serum starvation caused various nuclear abnormalities, which were similarly induced in T antigen-expressing T98G cells. Our present findings indicate that overexpression of HMGA1 disturbs RB-mediated cell arrest, suggesting a negative control of RB by HMGA1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.