ArticleCancer prevention research (Philadelphia, Pa.)2010
A vitamin D receptor-alkylating derivative of 1α,25-dihydroxyvitamin D3 inhibits growth of human kidney cancer cells and suppresses tumor growth.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Vitamin D-binding protein, circulating vitamin D and risk of renal cell carcinoma.International journal of cancer · 2014Trial
- Therapeutic implications of vitamin D in leukemia: mechanistic and clinical perspectives.Medical oncology (Northwood, London, England) · 2025Review
- Vitamin D in Cancer Prevention and Treatment: A Review of Epidemiological, Preclinical, and Cellular Studies.Cancers · 2024Review
- Article
- [Correlation between 25-hydroxyvitamin D and nephroblastoma in children and its value in assessing disease prognosis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases.Current medicinal chemistry · 2018Review
- PRL-3 engages the focal adhesion pathway in triple-negative breast cancer cells to alter actin structure and substrate adhesion properties critical for cell migration and invasion.Cancer letters · 2016Article
- Genome-wide functional genetic screen with the anticancer agent AMPI-109 identifies PRL-3 as an oncogenic driver in triple-negative breast cancers.Oncotarget · 2016Article
- Vitamin D and urological cancers.Central European journal of urology · 2016Review
- The future of vitamin D analogs.Frontiers in physiology · 2014Review
- 1α,25-Dihydroxyvitamin D3-3β-bromoacetate, a potential cancer therapeutic agent: synthesis and molecular mechanism of action.Bioorganic & medicinal chemistry letters · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
1,25-Dihydroxyvitamin D₃ [1,25(OH)₂D₃] has shown strong promise as an antiproliferative agent in several malignancies, yet its therapeutic use has been limited by its toxicity leading to search for analogues with antitumor property and low toxicity. In this study, we evaluated the in vitro and in vivo properties of 1,25-dihydroxyvitamin D₃-3-bromoacetate [1,25(OH)₂D₃-3-BE], an alkylating derivative of 1,25(OH)₂D₃, as a potential therapeutic agent for renal cancer. Dose response of 1,25(OH)₂D₃-3-BE in 2 kidney cancer cell lines was evaluated for its antiproliferative and apoptotic properties, and mechanisms were evaluated by Western blot and FACS analyses. Therapeutic potential of 1,25(OH)₂D₃-3-BE was assessed both by determining its stability in human serum and by evaluating its efficacy in a mouse xenograft model of human renal tumor. We observed that 1,25(OH)₂D₃-3-BE is significantly more potent than an equivalent concentration of 1,25(OH)₂D₃ in inhibiting growth of A498 and Caki 1 human kidney cancer cells. 1,25(OH)₂D₃-3-BE-mediated growth inhibition was promoted through inhibition of cell-cycle progression by downregulating cyclin A and induction of apoptosis by stimulating caspase activity. Moreover, 1,25(OH)₂D₃-3-BE strongly inhibited Akt phosphorylation and phosphorylation of its downstream target, caspase-9. 1,25(OH)₂D₃-3-BE seemed to be stable in human serum. In xenograft mouse model of human renal tumor, 1,25(OH)₂D₃-3-BE was more potent at reducing tumor size than 1,25(OH)₂D₃, which was accompanied by an increase in apopotosis and reduction of cyclin A staining in the tumors. These results suggest a translational potential of this compound as a therapeutic agent in renal cell carcinoma. Data from this study and extensive studies of vitamin D for the prevention of many malignancies support the potential of 1,25(OH)₂D₃-3-BE for preventing renal cancer and the development of relevant in vivo prevention models for assessing this potential, which do not exist at present.
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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.