ArticleOncogene2010
Transcriptional factor HBP1 targets P16(INK4A), upregulating its expression and consequently is involved in Ras-induced premature senescence.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- p38 mitogen-activated protein kinase drives senescence in CD4Immunity & ageing : I & A · 2025Article
- Unlocking mitochondrial dysfunction-associated senescence (MiDAS) with NADTranslational oncology · 2024Article
- The transcription factor HBP1 promotes ferroptosis in tumor cells by regulating the UHRF1-CDO1 axis.PLoS biology · 2023Article
- HBP1 inhibits the development of type 2 diabetes mellitus through transcriptional activation of theAging · 2022Article
- Methylation of HBP1 by PRMT1 promotes tumor progression by regulating actin cytoskeleton remodeling.Oncogenesis · 2022Article
- Structural and Functional Insights into GID/CTLH E3 Ligase Complexes.International journal of molecular sciences · 2022Review
- Targeting the MDM2-p53 pathway in dedifferentiated liposarcoma.Frontiers in oncology · 2022Review
- Transcriptional regulation of INK4/ARF locus by cis and trans mechanisms.Frontiers in cell and developmental biology · 2022Review
- HBP1-mediated transcriptional repression of AFP inhibits hepatoma progression.Journal of experimental & clinical cancer research : CR · 2021Article
- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Senescent T cells within suppressive tumor microenvironments: emerging target for tumor immunotherapy.The Journal of clinical investigation · 2020Review
- Article
- The HMG box transcription factor HBP1: a cell cycle inhibitor at the crossroads of cancer signaling pathways.Cellular and molecular life sciences : CMLS · 2019Review
- Article
- MiR-21 improves invasion and migration of drug-resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1.Cancer medicine · 2018Article
- Baicalein and baicalin inhibit colon cancer using two distinct fashions of apoptosis and senescence.Oncotarget · 2018Article
- Increased mediator complex subunit 15 expression is associated with poor prognosis in hepatocellular carcinoma.Oncology letters · 2018Article
- HMG-box transcription factor 1: a positive regulator of the G1/S transition through the Cyclin-CDK-CDKI molecular network in nasopharyngeal carcinoma.Cell death & disease · 2018Article
- The Role of p16International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Oncogene-mediated premature senescence has emerged as a potential tumor-suppressive mechanism in early cancer transitions. Many studies showed that Ras and p38 mitogen-activated protein kinase (MAPK) participate in premature senescence. Our previous work indicated that the HMG box-containing protein 1 (HBP1) transcription factor is involved in Ras- and p38 MAPK-induced premature senescence, but the mechanism of which has not yet been identified. Here, we showed that the p16(INK4A) cyclin-dependent kinase inhibitor is a novel target of HBP1 participating in Ras-induced premature senescence. The promoter of the p16(INK4A) gene contains an HBP1-binding site at position -426 to -433 bp from the transcriptional start site. HBP1 regulates the expression of the endogenous p16(INK4A) gene through direct sequence-specific binding. With HBP1 expression and the subsequent increase of p16(INK4A) gene expression, Ras induces premature senescence in primary cells. The data suggest a model in which Ras and p38 MAPK signaling engage HBP1 and p16(INK4A) to trigger premature senescence. In addition, we report that HBP1 knockdown is also required for Ras-induced transformation. All the data indicate that the mechanism of HBP1-mediated transcriptional regulation is important for not only premature senescence but also tumorigenesis.
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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.