ArticleCancer research2012
Contrasting behavior of the p18INK4c and p16INK4a tumor suppressors in both replicative and oncogene-induced senescence.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- An integrative analysis based on multiple cell death patterns identifies an immunosuppressive subtype and establishes a prognostic signature in lower-grade glioma.Annals of medicine · 2024Article
- Comprehensive analysis of senescence-related genes and immune infiltration in intervertebral disc degeneration: a meta-data approach utilizing bulk and single-cell RNA sequencing data.Frontiers in molecular biosciences · 2023Article
- Comprehensive analysis of the cancer driver genes constructs a seven-gene signature for prediction of survival and tumor immunity in hepatocellular carcinoma.Frontiers in genetics · 2022Article
- Antineoplastic Effects of Ankaferd Hemostat.BioMed research international · 2022Review
- Convergence of therapy-induced senescence (TIS) and EMT in multistep carcinogenesis: current opinions and emerging perspectives.Cell death discovery · 2020Review
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.PLoS biology · 2017Article
- Proteomic and transcriptomic analyses to explain the pleiotropic effects of Ankaferd blood stopper.SAGE open medicine · 2017Review
- A Conserved Gammaherpesvirus Cyclin Specifically Bypasses Host p18(INK4c) To Promote Reactivation from Latency.Journal of virology · 2015Article
- Evidence for a CDK4-dependent checkpoint in a conditional model of cellular senescence.Cell cycle (Georgetown, Tex.) · 2015Article
- Genome-wide co-localization of Polycomb orthologs and their effects on gene expression in human fibroblasts.Genome biology · 2014Article
- Cell cycle regulation by long non-coding RNAs.Cellular and molecular life sciences : CMLS · 2013Review
- CDK4/6-inhibiting drug substitutes for p21 and p16 in senescence: duration of cell cycle arrest and MTOR activity determine geroconversion.Cell cycle (Georgetown, Tex.) · 2013Article
- Canonical TGF-β pathway activity is a predictor of SHH-driven medulloblastoma survival and delineates putative precursors in cerebellar development.Brain pathology (Zurich, Switzerland) · 2013Article
- Management of gastric carcinoids (neuroendocrine neoplasms).Current gastroenterology reports · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The cyclin-dependent kinase (CDK) inhibitors, p18(INK4c) and p16(INK4a), both have the credentials of tumor suppressors in human cancers and mouse models. For p16(INK4a), the underlying rationale is its role in senescence, but the selective force for inactivation of p18(INK4c) in incipient cancer cells is less clear. Here, we show that in human fibroblasts undergoing replicative or oncogene-induced senescence, there is a marked decline in the levels of p18(INK4c) protein and RNA, which mirrors the accumulation of p16(INK4a). Downregulation of INK4c is not dependent on p16(INK4a), and RAS can promote the loss of INK4c without cell-cycle arrest. Downregulation of p18(INK4c) correlates with reduced expression of menin and E2F1 but is unaffected by acute cell-cycle arrest or inactivation of the retinoblastoma protein (pRb). Collectively, our data question the idea that p18(INK4c) acts as a backup for loss of p16(INK4a) and suggest that the apparent activation of p18(INK4c) in some settings represents delayed senescence rather than increased expression. We propose that the contrasting behavior of the two very similar INK4 proteins could reflect their respective roles in senescence versus differentiation.
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What OpenQuestion holds
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.