ArticleHematological oncology2010
Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors.
Article in Hematological oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Roles of Glutathione and AP-1 in the Enhancement of Vitamin D-Induced Differentiation by Activators of the Nrf2 Signaling Pathway in Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2024Article
- Silibinin: an old drug for hematological disorders.Oncotarget · 2017Review
- BRAF signals to pro-apoptotic BIM to enhance AraC cytotoxicity induced in AML cells by Vitamin D-based differentiation agents.The Journal of steroid biochemistry and molecular biology · 2017Article
- Established Human Cell Lines as Models to Study Anti-leukemic Effects of Flavonoids.Current genomics · 2017Article
- Prodifferentiation Activity of Novel Vitamin D₂ Analogs PRI-1916 and PRI-1917 and Their Combinations with a Plant Polyphenol in Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2016Article
- The role of VDR and BIM in potentiation of cytarabine-induced cell death in human AML blasts.Oncotarget · 2016Article
- The Potential of Vitamin D-Regulated Intracellular Signaling Pathways as Targets for Myeloid Leukemia Therapy.Journal of clinical medicine · 2015Review
- The MAPK ERK5, but not ERK1/2, inhibits the progression of monocytic phenotype to the functioning macrophage.Experimental cell research · 2015Article
- ERK5 pathway regulates transcription factors important for monocytic differentiation of human myeloid leukemia cells.Journal of cellular physiology · 2014Article
- Cell-Type-Specific Effects of Silibinin on Vitamin D-Induced Differentiation of Acute Myeloid Leukemia Cells Are Associated with Differential Modulation of RXRα Levels.Leukemia research and treatment · 2012Article
- Oncoprotein Cot1 represses kinase suppressors of Ras1/2 and 1,25-dihydroxyvitamin D3-induced differentiation of human acute myeloid leukemia cells.Journal of cellular physiology · 2011Article
- The Nrf2 transcription factor is a positive regulator of myeloid differentiation of acute myeloid leukemia cells.Cancer biology & therapy · 2011Article
- Isoforms of p38MAPK gamma and delta contribute to differentiation of human AML cells induced by 1,25-dihydroxyvitamin D₃.Experimental cell research · 2011Article
- RB in breast cancer: differential effects in estrogen receptor-positive and estrogen receptor-negative disease.Cell cycle (Georgetown, Tex.) · 2010Article
- Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D(3).Cell cycle (Georgetown, Tex.) · 2010Article
- Role of Silymarin in Cancer Treatment: Facts, Hypotheses, and Questions.Journal of evidence-based integrative medicineReview
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Induction of terminal differentiation is a conceptually attractive approach for the therapy of neoplastic diseases. Although vitamin D derivatives (deltanoids) can induce differentiation of AML cells in vitro, so far deltanoids have not been successfully brought to the clinic, due to the likelihood of life-threatening hypercalcemia. Here, we incubated freshly obtained blood cells from patients with AML with a plant antioxidant (PAOx), silibinin (SIL), alone or together with a deltanoid. Twenty patients with AML (all subtypes except M3) were available for this study, and in 14 (70%), SIL (60 µM) either induced differentiation ex vivo, or enhanced differentiation induced by deltanoids, or both. Interestingly, SIL acting alone induced differentiation only in cases in which chromosome aberrations could not be detected. In eleven samples sufficient material was available for a limited analysis of the underlying events. Quantitative RT-PCR showed that differentiation markers were upregulated at the mRNA level by both SIL and deltanoids, suggesting that intracellular signaling pathways upstream of transcription factors (TFs) were activated by these agents. Western analysis for proteins which function as TFs in deltanoid-induced monocytic differentiation, such as members of Jun and C/EBP families, surprisingly demonstrated that SIL upregulated all these TFs in the cases tested. This suggests that although the presence of SIL may not always be sufficient to induce differentiation, it can serve as a differentiation enabling factor for blasts obtained from a large proportion of patients with AML. Thus, SIL/deltanoid combinations warrant further consideration as preventive/therapeutic regimens in human leukaemia.
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