ArticleCellular and molecular life sciences : CMLS2011
Role of p21 in SP600125-induced cell cycle arrest, endoreduplication, and apoptosis.
Article in Cellular and molecular life sciences : CMLS, 2011. 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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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Subcellular compartmentalization dependent dichotomy of p21 in cancer.Molecular biology reports · 2026Review
- Human menstrual blood-derived stem cells alleviate autoimmune hepatitis via JNK/MAPK signaling pathway in vivo and in vitro.Frontiers of medicine · 2023Article
- A New Method for Chromosomes Preparation by ATP-Competitive Inhibitor SP600125Frontiers in bioengineering and biotechnology · 2020Article
- 17-DMAG regulates p21 expression to induce chondrogenesisDisease models & mechanisms · 2018Article
- AKT is indispensable for coordinating Par-4/JNK cross talk in p21 downmodulation during ER stress.Oncogenesis · 2017Article
- JNK Inhibition Inhibits Lateral Line Neuromast Hair Cell Development.Frontiers in cellular neuroscience · 2016Article
- SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways.Oncotarget · 2015Article
- SP600125 induces Src and type I IGF receptor phosphorylation independent of JNK.International journal of molecular sciences · 2014Article
- PI3K-AKT-mTOR-signaling and beyond: the complex network in gastroenteropancreatic neuroendocrine neoplasms.Theranostics · 2014Review
- Inhibition of c-Jun NH2-terminal kinase stimulates mu opioid receptor expression via p38 MAPK-mediated nuclear NF-κB activation in neuronal and non-neuronal cells.Biochimica et biophysica acta · 2013Article
- Cholinergic precursors modulate the expression of heme oxigenase-1, p21 during astroglial cell proliferation and differentiation in culture.Neurochemical research · 2012Article
- Investigating the role of c-Jun N-terminal kinases in the proliferation of Werner syndrome fibroblasts using diaminopyridine inhibitors.Chemistry Central journal · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-cancer effect of the c-Jun N-terminal kinase (JNK) inhibitor SP600125 has been well evaluated in human cancer cells. However the role of p21 in SP600125-mediated G(2)/M distribution is not fully understood. Our results showed that the transcriptional activation of p21 by SP600125 is mediated through the proximal regions of multiple Sp1 sites in the p21 promoter following ERK-dependent phosphorylation of Sp1. In this process, p21 induces endoreduplication through the inhibition of cyclin E/Cdk2 activity at 24 h but does not directly regulate cyclin B1/Cdc2 activity. Furthermore, SP600125 induces the phosphorylation of p21 at Thr 145 through the PI3K/Akt pathway. Akt-mediated phosphorylation of p21 and protection of apoptosis are completely abolished by inhibitors of PI3K and Akt. In summary using time points, we identified the dual functions of p21 as an inhibitor of cell-cycle progression at 24 h and as an anti-apoptotic factor at 48 h.
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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.