ArticleThe Journal of biological chemistry2011
A dormant state modulated by osmotic pressure controls clonogenicity of prostate cancer cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Physical Forces in Glioblastoma Migration: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Mechanistic target of rapamycin (mTOR) regulates self-sustained quiescence, tumor indolence, and late clinical metastasis in a Beclin-1-dependent manner.Cell cycle (Georgetown, Tex.) · 2023Article
- Tumorigenic mesenchymal clusters are less sensitive to moderate osmotic stresses due to low amounts of junctional E-cadherin.Scientific reports · 2021Article
- Osmotic pressure modulates single cell cycle dynamics inducing reversible growth arrest and reactivation of human metastatic cells.Scientific reports · 2021Article
- Sodium homeostasis in the tumour microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Transient exposure to androgens induces a remarkable self-sustained quiescent state in dispersed prostate cancer cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Physical activity and its mechanistic effects on prostate cancer.Prostate cancer and prostatic diseases · 2015Review
- SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy.Cell cycle (Georgetown, Tex.) · 2015Article
- Follistatin as potential therapeutic target in prostate cancer.Targeted oncology · 2013Review
- Clinical and Therapeutic Implications of Follistatin in Solid Tumours.Cancer genomics & proteomicsReview
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell dormancy constitutes a limiting step of the metastatic process by preventing the proliferation of isolated cancer cells disseminated at distant sites from the primary tumor. The study of cancer cell dormancy is severely hampered by the lack of biological samples so that the mechanisms that regulate cell dormancy have not been extensively explored. In this work, we describe the rapid induction in vitro of a dormant state in prostate cancer cells by exposure to a slightly hypertonic growth medium. This quiescence is observed only when cells are seeded at low density and, once established, requires additional stimuli besides osmotic pressure to be reversed. Media conditioned by cells grown at high density can partially prevent or reverse dormancy, a phenomenon which can be reproduced with citric acid. In addition to this role of small metabolites, inactivation of the p53 and smad pathways also counters the entry into dormancy, whereas exposure to activin A induces it to some extent. Thus, this easily inducible dormancy reproduces several features associated with the dormancy of stem cells and cancer cells in vivo.
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