ArticleOncotarget2016
ROCK inhibitor reduces Myc-induced apoptosis and mediates immortalization of human keratinocytes.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
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- Fibroblast stromal support model for predicting human papillomavirus-associated cancer drug responses.Journal of virology · 2024Article
- Fibroblasts Regulate the Transformation Potential of Human Papillomavirus-positive Keratinocytes.bioRxiv : the preprint server for biology · 2024Article
- Rho Kinases and Reactive Oxygen Species in Autophagy Regulation by Pressure in Periodontal Ligament Cells.Brazilian dental journal · 2024Article
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- Rho Kinases in Embryonic Development and Stem Cell Research.Archivum immunologiae et therapiae experimentalis · 2022Review
- RAS induced senescence of skin keratinocytes is mediated through Rho-associated protein kinase (ROCK).Molecular carcinogenesis · 2021Article
- Immortalization and Characterization of Rat Lingual Keratinocytes in a High-Calcium and Feeder-Free Culture System Using ROCK Inhibitor Y-27632.International journal of molecular sciences · 2021Article
- Conditional reprogramming culture conditions facilitate growth of lower-grade glioma models.Neuro-oncology · 2021Article
- An overview of neuroblastoma cell lineage phenotypes andExperimental biology and medicine (Maywood, N.J.) · 2020Review
- Conditional reprogramming: next generation cell culture.Acta pharmaceutica Sinica. B · 2020Review
- Conditional reprogramming: Modeling urological cancer and translation to clinics.Clinical and translational medicine · 2020Review
- Culture and application of conditionally reprogrammed primary tumor cells.Gastroenterology report · 2020Review
- Efficient correction of a deleterious point mutation in primary horse fibroblasts with CRISPR-Cas9.Scientific reports · 2020Article
- Murine neuroblastoma cell lines developed by conditional reprogramming preserve heterogeneous phenotypes observed in vivo.Laboratory investigation; a journal of technical methods and pathology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
The Myc/Max/Mad network plays a critical role in cell proliferation, differentiation and apoptosis and c-Myc is overexpressed in many cancers, including HPV-positive cervical cancer cell lines. Despite the tolerance of cervical cancer keratinocytes to high Myc expression, we found that the solitary transduction of the Myc gene into primary cervical and foreskin keratinocytes induced rapid cell death. These findings suggested that the anti-apoptotic activity of E7 in cervical cancer cells might be responsible for negating the apoptotic activity of over-expressed Myc. Indeed, our earlier in vitro studies demonstrated that Myc and E7 synergize in the immortalization of keratinocytes. Since we previously postulated that E7 and the ROCK inhibitor, Y-27632, were members of the same functional pathway in cell immortalization, we tested whether Y-27632 would inhibit apoptosis induced by the over-expression of Myc. Our findings indicate that Y-27632 rapidly inhibited Myc-induced membrane blebbing and cellular apoptosis and, more generally, functioned as an inhibitor of extrinsic and intrinsic pathways of cell death. Most important, Y-27632 cooperated with Myc to immortalize keratinocytes efficiently, indicating that apoptosis is a major barrier to Myc-induced immortalization of keratinocytes. The anti-apoptotic activity of Y-27632 correlated with a reduction in p53 serine 15 phosphorylation and the consequent reduction in the expression of downstream target genes p21 and DAPK1, two genes involved in the induction of cell death.
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