Expression of vitamin D receptor (VDR), cyclooxygenase-2 (COX-2) and 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in benign and malignant ovarian tissue and 25-hydroxycholecalciferol (25(OH2)D3) and prostaglandin E2 (PGE2) serum level in ovarian cancer patients

Thill, Marc; Fischer, Dorothea; Kelling, Katharina; Hoellen, Friederike; Dittmer, C.; Hornemann, Amadeus; Salehin, Darius; Diedrich, K.; Friedrich, Michael; Becker, Steffi

doi:10.1016/j.jsbmb.2010.03.049

Cited by 42 publications

(30 citation statements)

References 13 publications

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“…In particular, VDRs were frequently expressed in benign lesions (93.5%) while in carcinoma in situ or in metastatic tumor the rate of expression was lower (56.2%) (Lopes et al, 2010). Similar results were obtained from studies which evaluated the expression level of VDR in benign and malignant ovarian tissues (Thill et al, 2010). These studies showed that VDR expression levels were significantly lower in malignant tissue as compared with normal tissue.…”

Section: Effects Of Cancer On Vdr Levelssupporting

confidence: 75%

Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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Context: There is increasing evidence that Vitamin D (Vit D) and its metabolites, besides their well-known calcium-related functions, may also exert antiproliferative, pro-differentiating, and immune modulatory effects on tumor cells in vitro and may also delay tumor growth in vivo. Objective: The aim of this review is to provide fresh insight into the most recent advances on the role of Vit D and its analogues as chemopreventive drugs in cancer therapy. Methods: A systematic review of experimental and clinical studies on Vit D and cancer was undertaken by using the major electronic health database including ISI Web of Science, Medline, PubMed, Scopus and Google Scholar. Results and conclusion: Experimental and clinical observations suggest that Vit D and its analogues may be effective in preventing the malignant transformation and/or the progression of various types of human tumors including breast cancer, prostate cancer, colorectal cancer, and some hematological malignances. These findings suggest the possibility of the clinical use of these molecules as novel potential chemopreventive and anticancer agents.

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Section: Effects Of Cancer On Vdr Levelssupporting

confidence: 75%

Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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“…Down-regulation of HPGD contributes to PGE2 accumulation in lung, colon, and pancreatic cancers (Pham et al, 2010). But, HPGD protein level is higher in malignant ovarian tissue samples compared to normal tissue, which does not correlate with the former report (Thill et al, 2010). HPGD is up-regulated in leukemia cells after combination treatment with 5-azacytidine and scriptaid.…”

Section: Discussioncontrasting

confidence: 80%

Recovery of Genes Epigenetically Altered by the Histone Deacetylase Inhibitor Scriptaid and Demethylating Agent 5-Azacytidine in Human Leukemia Cells

Park¹,

Jeon²,

Kim³

et al. 2010

Genomics & Informatics

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Histone deacetylation and demethylation are epigenetic mechanisms implicated in cancer. Studies regarding the role of modulation of gene expression utilizing the histone deacetylase inhibitor scriptaid and the demethylating agent 5-azacytidine in HL-60 leukemia cells have been limited. We studied the possibility of recovering epigenetically silenced genes by scriptaid and 5-azacytidine in human leukemia cells by DNA microarray analysis. The first group was leukemia cells that were cultured with 5-azacytidine. The second group was cultured with scriptaid. The other group was cultured with both agents. Two hundred seventy newly developed genes were expressed after the combination of 5-azacytidine and scriptaid. Twenty-nine genes were unchanged after the combination treatment of 5-azacytidine and scriptaid. Among the 270 genes, 13 genes were differed significantly from the control. HPGD, CPA3, CEACAM6, LOC653907, ETS1, RAB37, PMP22, FST, FOXC1, and CCL2 were up-regulated, and IGLL3, IGLL1, and ASS1were down-regulated. Eleven genes associated with oncogenesis were found among the differentially expressed genes: ETS1, ASCL2, BTG2, BTG1, SLAMF6, CDKN2D, RRAS, RET, GIPC1, MAGEB, and RGL4. We report the results of our leukemia cell microarray profiles after epigenetic combination therapy with the hope that they are the starting point of selectively targeted epigenetic therapy.

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“…Several invitro and invivo studies on breast cancer and prostate cancer showed 1α 25(OH) 2 D 3 significantly decreases the expression of cyclooxygenase-2 (COX-2) and stimulates 15-PGDH levels (Krishnan & Feldman, 2011). However, several invivo studies showed the inverse correlation between VDR and both COX-2 and 15-Hydroxyprostaglandin Dehydrogenase (15-PGDH), as well as between PGE2 and 1α 25(OH) 2 D 3 levels suggests a possible link between VDR associated target genes and prostaglandin metabolism in breast cancer and ovarian cancer (Figure 3) (Thill et al, 2010a;2010b). Interestingly, a tight coupling between the expression of COX-2 and aromatase was observed in breast cancer patients (Brueggemeier et al, 1999;Brodie et al, 2001).…”

Section: Cyp24a1mentioning

confidence: 99%