1 alpha, 25-dihydroxylvitamin D3 promotes Bacillus Calmette-Guérin immunotherapy of bladder cancer

Hsu, Jong-Wei; Yin, Peng-Nien; Wood, Ronald; Messing, James; Messing, Edward M.; Lee, Yi-Fen

doi:10.18632/oncotarget.1494

Cited by 27 publications

(22 citation statements)

References 50 publications

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“…Previous studies suggest that vitamin D can inhibit proliferation and induce apoptosis in human bladder tumor cells in vitro [11,12,27]. The findings from the meta-analysis provide strong epidemiological evidence for the important role of vitamin D in bladder carcinogenesis.…”

Section: Discussionmentioning

confidence: 62%

Vitamin D Deficiency and Increased Risk of Bladder Carcinoma: A Meta-Analysis

Zhang

Wen

et al. 2015

Cell Physiol Biochem

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Background/Aims: Vitamin D status in relation to bladder carcinoma risk was still inconsistent. This study was carried out to evaluate the relationship between vitamin D status and bladder carcinoma risk through a meta-analysis approach. Methods: Pubmed, Web of Science, CNKI, and Embase were searched systemically to find eligible studies from the earliest available date to April 16, 2015. The search terms “vitamin D”, “25-hydroxyvitamin D”, “bladder cancer” or “bladder carcinoma” were used to retrieve relevant studies. The exposure of interest was intake of vitamin D or serum vitamin D levels, and the outcome of interest was bladder carcinoma incidence or mortality. The pooled risk ratio (RR) values and their 95%CIs were calculated through meta-analysis. Results: Seven studies with a total of 62,141 participants met the inclusion criteria and were finally included into the meta-analysis. There was no heterogeneity among those included studies (I² = 0%, P = 0.53). The pooled RR of bladder carcinoma for the lowest category versus the highest category of vitamin D was 1.34 (95% CI 1.17-1.53, P < 0.0001). Sensitivity analysis by omitting one study by turns showed all the pooled RRs were statistically significant. Meta-analysis of 5 studies reporting outcomes of serum vitamin D levels also showed that the low serum vitamin D level was associated with increased risk of bladder carcinoma (RR = 1.32, 95%CI 1.15-1.52, P = 0.0001). No obvious risk of publication bias was observed. Conclusion: Vitamin D deficiency is associated with increased risk of bladder carcinoma in present study.

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Section: Discussionmentioning

confidence: 62%

Vitamin D Deficiency and Increased Risk of Bladder Carcinoma: A Meta-Analysis

Zhang

Wen

et al. 2015

Cell Physiol Biochem

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“…As shown in Fig. 5C, all of the cell types display the VDR and thus may be responsible for the suppression of omental metastases by 1,25D 3 .1,25D 3 actions in adipocytes [28], fibroblasts [5] and immune cells [14,27] have been reported in the literature. Elucidation of the molecular mechanism underlying the suppression of EOC invasion mediated through stromal VDR relies on the identification of the main cell types in omental tumor microenvironment that mediate the 1,25D 3 action through the stromal VDR.…”

Section: Discussionmentioning

confidence: 99%

Suppression of epithelial ovarian cancer invasion into the omentum by 1α,25-dihydroxyvitamin D3 and its receptor

Lungchukiet

Sun

Kasiappan

et al. 2015

The Journal of Steroid Biochemistry and Molecular Biology

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Epithelial ovarian cancer (EOC) is the leading cause of gynecological cancer death in women, mainly because it has spread to intraperitoneal tissues such as the omentum in the peritoneal cavity by the time of diagnosis. In the present study, we established in vitro assays, ex vivo omental organ culture system and syngeneic animal tumor models using wild type (WT) and vitamin D receptor (VDR) null mice to investigate the effects of 1α,25-dihydroxyvitamin D3 (1,25D3) and VDR on EOC invasion. Treatment of human EOC cells with 1,25D3 suppressed their migration and invasion in monolayer scratch and transwell assays and ability to colonize the omentum in the ex vivo system, supporting a role for epithelial VDR in interfering with EOC invasion. Furthermore, VDR knockdown in OVCAR3 cells increased their ability to colonize the omentum in the ex vivo system in the absence of 1,25D3, showing a potential ligand-independent suppression of EOC invasion by epithelial VDR. In syngeneic models, ID8 tumors exhibited an increased ability to colonize omenta of VDR null over that of WT mice; pre-treatment of WT, not VDR null, mice with EB1089 reduced ID8 colonization, revealing a role for stromal VDR in suppressing EOC invasion. These studies are the first to demonstrate a role for epithelial and stromal VDR in mediating the activity of 1,25D3 as well as a 1,25D3-independent action of the VDR in suppressing EOC invasion. The data suggest that VDR-based drug discovery may lead to the development of new intervention strategies to improve the survival of patients with EOC at advanced stages. This article is part of a Special Issue entitled “Vitamin D Workshop”.

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“…A&B). Based on clinical BCG intravesical therapy guidelines and a previously published paper, we used BCG only or combined with ASC-J9 @ to treat BCa cell or intravesical therapy in BBN-induced BCa mouse model both for two hours (28), and the results showed that the combination of BCG and HF or ASC-J9 ® better suppressed BCa progression.…”

Section: Discussionmentioning

confidence: 99%

Antiandrogen Therapy with Hydroxyflutamide or Androgen Receptor Degradation Enhancer ASC-J9 Enhances BCG Efficacy to Better Suppress Bladder Cancer Progression

Shang

Zhang

et al. 2015

Molecular Cancer Therapeutics

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Recent studies suggested that the androgen receptor (AR) might play important roles to influence the bladder cancer (BCa) progression, yet its clinical application remains unclear. Here we developed a new combined therapy with Bacillus Calmette-Guérin (BCG) and the AR degradation enhancer ASC-J9® or anti-androgen hydroxyflutamide (HF) to better suppress the BCa progression. Mechanism dissection revealed that ASC-J9® treatment enhanced BCG efficacy to suppress BCa cell proliferation via increasing the recruitment of monocytes/macrophages that involved the promotion of BCG attachment/internalization to the BCa cells through increased integrin-α5β1 expression and IL-6 release. Such consequences might then enhance BCG-induced BCa cell death via increased TNF-α release. Interestingly, we also found ASC-J9® treatment could directly promote BCG-induced HMGB1 release to enhance the BCG cytotoxic effects for the suppression of BCa cell growth. In vivo approaches also concluded that ASC-J9® could enhance the BCG efficacy to better suppress the BCa progression in BBN-induced BCa mouse models. Together, these results suggest that the newly developed therapy combining BCG plusASC-J9® may become a novel therapy to better suppress BCa progress.

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1 alpha, 25-dihydroxylvitamin D3 promotes Bacillus Calmette-Guérin immunotherapy of bladder cancer

Cited by 27 publications

References 50 publications

Vitamin D Deficiency and Increased Risk of Bladder Carcinoma: A Meta-Analysis

Vitamin D Deficiency and Increased Risk of Bladder Carcinoma: A Meta-Analysis

Suppression of epithelial ovarian cancer invasion into the omentum by 1α,25-dihydroxyvitamin D3 and its receptor

Antiandrogen Therapy with Hydroxyflutamide or Androgen Receptor Degradation Enhancer ASC-J9 Enhances BCG Efficacy to Better Suppress Bladder Cancer Progression

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