ArticleExperimental cell research2010
Bmi-1 extends the life span of normal human oral keratinocytes by inhibiting the TGF-beta signaling.
Article in Experimental cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Efficient immortalization of primary nasopharyngeal epithelial cells for EBV infection study.PloS one · 2013Trial
- Ageing of the Oral Mucosa: Mechanisms and Consequences.International dental journal · 2026Review
- Epithelial cells release IL-36α in extracellular vesicles following mechanical damage.Biochemical and biophysical research communications · 2022Article
- Article
- miR-200c Modulates the Pathogenesis of Radiation-Induced Oral Mucositis.Oxidative medicine and cellular longevity · 2019Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
- P16Scientific reports · 2017Article
- MicroRNA-146a-5p Limits Elevated TGF-β Signal during Cell Senescence.Molecular therapy. Nucleic acids · 2017Article
- Activation of Wnt/β-catenin signaling by lithium chloride attenuates d-galactose-induced neurodegeneration in the auditory cortex of a rat model of aging.FEBS open bio · 2017Article
- Role of keratin 24 in human epidermal keratinocytes.PloS one · 2017Article
- Orai1 promotes tumor progression by enhancing cancer stemness via NFAT signaling in oral/oropharyngeal squamous cell carcinoma.Oncotarget · 2016Article
- A miR-200c/141-BMI1 autoregulatory loop regulates oncogenic activity of BMI1 in cancer cells.Oncotarget · 2016Article
- Orai1 mediates osteogenic differentiation via BMP signaling pathway in bone marrow mesenchymal stem cells.Biochemical and biophysical research communications · 2016Article
- The Role of ORAI1 in the Odontogenic Differentiation of Human Dental Pulp Stem Cells.Journal of dental research · 2015Article
- Regulation of p53 during senescence in normal human keratinocytes.Aging cell · 2015Article
- MicroRNA-31 is a transcriptional target of histone deacetylase inhibitors and a regulator of cellular senescence.The Journal of biological chemistry · 2015Article
- PLK1 inhibition down-regulates polycomb group protein BMI1 via modulation of the miR-200c/141 cluster.The Journal of biological chemistry · 2015Article
- Gene expression signatures affected by ethanol and/or nicotine in normal human normal oral keratinocytes (NHOKs).Genomics data · 2014Article
- Bmi-1 plays a critical role in protection from renal tubulointerstitial injury by maintaining redox balance.Aging cell · 2014Article
- microRNA-141 regulates BMI1 expression and induces senescence in human diploid fibroblasts.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We previously demonstrated that Bmi-1 extended the in vitro life span of normal human oral keratinocytes (NHOK). We now report that the prolonged life span of NHOK by Bmi-1 is, in part, due to inhibition of the TGF-beta signaling pathway. Serial subculture of NHOK resulted in replicative senescence and terminal differentiation and activation of TGF-beta signaling pathway. This was accompanied with enhanced intracellular and secreted TGF-beta1 levels, phosphorylation of Smad2/3, and increased expression of p15(INK4B) and p57(KIP2). An ectopic expression of Bmi-1 in NHOK (HOK/Bmi-1) decreased the level of intracellular and secreted TGF-beta1 induced dephosphorylation of Smad2/3, and diminished the level of p15(INK4B) and p57(KIP2). Moreover, Bmi-1 expression led to the inhibition of TGF-beta-responsive promoter activity in a dose-specific manner. Knockdown of Bmi-1 in rapidly proliferating HOK/Bmi-1 and cancer cells increased the level of phosphorylated Smad2/3, p15(INK4B), and p57(KIP2). In addition, an exposure of senescent NHOK to TGF-beta receptor I kinase inhibitor or anti-TGF-beta antibody resulted in enhanced replicative potential of cells. Taken together, these data suggest that Bmi-1 suppresses senescence of cells by inhibiting the TGF-beta signaling pathway in NHOK.
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Registered trials
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