ArticleThe Biochemical journal2003
Cell-cycle arrest in Jurkat leukaemic cells: a possible role for docosahexaenoic acid.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 66 citations in OpenAlex.
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- The doxorubicin-induced cell motility network is under the control of the ceramide-activated protein phosphatase 1 alpha.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Inhibition of Phosphatidylinositol 3-kinase (PI3K) Signaling Synergistically Potentiates Antitumor Efficacy of Paclitaxel and Overcomes Paclitaxel-Mediated Resistance in Cervical Cancer.International journal of molecular sciences · 2019Article
- Effects of the polyunsaturated fatty acids, EPA and DHA, on hematological malignancies: a systematic review.Oncotarget · 2018Review
- A Critical Review on the Effect of Docosahexaenoic Acid (DHA) on Cancer Cell Cycle Progression.International journal of molecular sciences · 2017Review
- Preparation of coffee oil-algae oil-based nanoemulsions and the study of their inhibition effect on UVA-induced skin damage in mice and melanoma cell growth.International journal of nanomedicine · 2017Article
- Different effects of omega-3 fatty acids on the cell cycle in C2C12 myoblast proliferation.Molecular and cellular biochemistry · 2012Article
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- Lipids, mitochondria and cell death: implications in neuro-oncology.Molecular neurobiology · 2010Review
- Protection by D609 through cell-cycle regulation after stroke.Molecular neurobiology · 2010Article
- Moderate strength (0.23-0.28 T) static magnetic fields (SMF) modulate signaling and differentiation in human embryonic cells.BMC genomics · 2009Article
- Docosahexaenoic acid sensitizes Ramos cells to Gamma-irradiation-induced apoptosis through involvement of PPAR-gamma activation and NF-kappaB suppression.Molecular and cellular biochemistry · 2008Article
- Involvement of PPAR-gamma and p53 in DHA-induced apoptosis in Reh cells.Molecular and cellular biochemistry · 2007Article
- 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazole acts in a reactive oxygen species-dependent manner to suppress human lung cancer growth.Journal of cancer research and clinical oncology · 2006Article
- Activation of serine/threonine protein phosphatase-1 is required for ceramide-induced survival of sympathetic neurons.The Biochemical journal · 2005Article
- Effects of EPA and DHA on proliferation, cytokine production, and gene expression in Raji cells.Lipids · 2004Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Docosahexaenoic acid (DHA) is known to have anti-cancer activities by mechanisms that are not well understood. In the present study, we test one possible pathway for DHA action in Jurkat leukaemic cells. Low doses of DHA (10 microM) are shown to induce cell-cycle arrest, whereas higher doses are cytotoxic. However, when cells that were pre-treated with 10 microM DHA are given an additional 10 microM DHA dose, cell viability rapidly decreases. Immunoblotting reveals that repeated low doses of DHA results in activation of caspase 3, implying induction of apoptosis. DHA (10 microM) is shown to increase ceramide levels after 6 h of incubation and, after 24 h, the cells appear to be arrested in S phase. With DHA, the amount of phosphorylated retinoblastoma protein (pRb) decreases significantly. Western blot analysis also shows that DHA greatly reduces the level of cyclin A, while increasing the level of p21 WAF1, a cellular inhibitor of cyclin A/cyclin-dependent kinase 2 (cdk2) activity. Furthermore, the observed DHA-induced doubling of the ratio of hypophosphorylated pRb (hypo-pRb) to total pRb is inhibited by tautomycin and phosphatidic acid (PA), known inhibitors of protein phosphatase 1 (PP1), and by the PP2 inhibitor okadaic acid. The present study demonstrates one possible connected pathway for DHA action. By this pathway, low doses of DHA increase ceramide levels, which leads to inhibition of cdk2 activity and stimulation of PP1 and PP2A. The net effect of cdk2 inhibition and protein phosphatase activation is an inhibition of pRb phosphorylation, consequently arresting Jurkat cell growth.
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