ArticleMolecular cancer research : MCR2010
p53-dependent induction of prostate cancer cell senescence by the PIM1 protein kinase.
Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
- CBX7 regulates chemotherapy-induced senescence-like growth arrest in multiple myeloma via the ERK/STAT3/PIM1 axis.Journal of translational medicine · 2025Article
- Fumiquinazolines F and G from the FungusInternational journal of molecular sciences · 2025Article
- REDD1 is a determinant of the sensitivity of renal cell carcinoma cells to autophagy inhibition that can be therapeutically exploited by targeting PIM activity.Cancer letters · 2025Article
- PIM1 induces hypoxia-related fibroblast senescence in a mouse model of stress urinary incontinence.PloS one · 2025Article
- The landscape of human tissue and cell type specific expression and co-regulation of senescence genes.Molecular neurodegeneration · 2022Article
- c-MYC and p53 expression highlight starry-sky pattern as a favourable prognostic feature in R-CHOP-treated diffuse large B-cell lymphoma.The journal of pathology. Clinical research · 2021Article
- Article
- The Oncogene PIM1 Contributes to Cellular Senescence by Phosphorylating Staphylococcal Nuclease Domain-Containing Protein 1 (SND1).Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Pim1 promotes cell proliferation and regulates glycolysis via interaction with MYC in ovarian cancer.OncoTargets and therapy · 2018Article
- Thyroid hormone inhibits growth of hepatoma cells through induction of miR-214.Scientific reports · 2017Article
- Article
- A positive feedback loop between Pim-1 kinase and HBP1 transcription factor contributes to hydrogen peroxide-induced premature senescence and apoptosis.The Journal of biological chemistry · 2017Article
- Transient exposure to androgens induces a remarkable self-sustained quiescent state in dispersed prostate cancer cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Interferon inducible antiviral MxA is inversely associated with prostate cancer and regulates cell cycle, invasion and Docetaxel induced apoptosis.The Prostate · 2015Article
- Article
- PIM-1 modulates cellular senescence and links IL-6 signaling to heterochromatin formation.Aging cell · 2014Article
- Tumor Protein 53-Induced Nuclear Protein 1 Enhances p53 Function and Represses Tumorigenesis.Frontiers in genetics · 2013Article
- Conditional transgenic expression of PIM1 kinase in prostate induces inflammation-dependent neoplasia.PloS one · 2013Article
- Network modeling of CDF treated pancreatic cancer cells reveals a novel c-myc-p73 dependent apoptotic mechanism.American journal of translational research · 2011Article
- The BH3 mimetic ABT-737 induces cancer cell senescence.Cancer research · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The PIM family of serine threonine protein kinases plays an important role in regulating both the growth and transformation of malignant cells. However, in a cell line-dependent manner, overexpression of PIM1 can inhibit cell and tumor growth. In 22Rv1 human prostate cells, but not in Du145 or RWPE-2, PIM1 overexpression was associated with marked increases in cellular senescence, as shown by changes in the levels of beta-galactosidase (SA-beta-Gal), p21, interleukin (IL)-6 and IL-8 mRNA and protein. During early cell passages, PIM1 induced cellular polyploidy. As the passage number increased, markers of DNA damage, including the level of gammaH2AX and CHK2 phosphorylation, were seen. Coincident with these DNA damage markers, the level of p53 protein and genes transcriptionally activated by p53, such as p21, TP53INP1, and DDIT4, increased. In these 22Rv1 cells, the induction of p53 protein was associated not only with senescence but also with a significant level of apoptosis. The importance of the p53 pathway to PIM1-driven cellular senescence was further shown by the observation that expression of dominant-negative p53 or shRNA targeting p21 blocked the PIM1-induced changes in the DNA damage response and increases in SA-beta-Gal activity. Likewise, in a subcutaneous tumor model, PIM1-induced senescence was rescued when the p53-p21 pathways are inactivated. Based on these results, PIM1 will have its most profound effects on tumorigenesis in situations where the senescence response is inactivated.
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