ArticleCell cycle (Georgetown, Tex.)2010
HdmX overexpression inhibits oncogene induced cellular senescence.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Targeting MDM4 as a Novel Therapeutic Approach in Prostate Cancer Independent of p53 Status.Cancers · 2022Article
- MDM2 turnover and expression of ATRX determine the choice between quiescence and senescence in response to CDK4 inhibition.Oncotarget · 2015Article
- Article
- FL118 induces p53-dependent senescence in colorectal cancer cells by promoting degradation of MdmX.Cancer research · 2014Article
- SIRT1 promotes proliferation and inhibits the senescence-like phenotype in human melanoma cells.Oncotarget · 2014Article
- Rapamycin induces pluripotent genes associated with avoidance of replicative senescence.Cell cycle (Georgetown, Tex.) · 2013Article
- MDM2, MDMX and p53 in oncogenesis and cancer therapy.Nature reviews. Cancer · 2013Review
- Ectopic NGAL expression can alter sensitivity of breast cancer cells to EGFR, Bcl-2, CaM-K inhibitors and the plant natural product berberine.Cell cycle (Georgetown, Tex.) · 2012Article
- Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.Oncotarget · 2012Review
- Mutations and deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades which alter therapy response.Oncotarget · 2012Review
- Oncogenic functions of hMDMX in in vitro transformation of primary human fibroblasts and embryonic retinoblasts.Molecular cancer · 2011Article
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is an irreversible state of terminal growth arrest that requires functional p53. Acting to block tumor formation, induction of senescence has also been demonstrated to contribute to tumor clearance via the immune system following p53 reactivation. The Hdm2-antagonist, Nutlin-3a, has been shown to reactivate p53 and induce a quiescent state in various cancer cell lines, similar to the G(1) arrest observed upon RNAi targeting of Hdm2 in MCF7 breast cancer. In the present study we show that HdmX, a negative regulator of p53, impacts the senescence pathway. Specifically, overexpression of HdmX blocks Ras mediated senescence in primary human fibroblasts. The interaction of HdmX with p53 and the re-localization of HdmX to the nucleus through Hdm2 association appear to be required for this activity. Furthermore, inhibiting HdmX in prostate adenocarcinoma cells expressing wild-type p53, mutant Ras and high levels of HdmX induced cellular senescence as measured by an increase in irreversible b-galactosidase staining. Together these results suggest that HdmX overexpression may contribute to tumor formation by blocking senescence and that targeting HdmX may represent an attractive anti-cancer therapeutic approach.
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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.