A combination of desmopressin and docetaxel inhibit cell proliferation and invasion mediated by urokinase-type plasminogen activator (uPA) in human prostate cancer cells

Sasaki, Hiroshi; Klotz, Laurence; Sugar, Linda; Kiss, Alexander; Venkateswaran, Vasundara

doi:10.1016/j.bbrc.2015.07.050

Cited by 24 publications

(34 citation statements)

References 20 publications

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“…Likewise, a biphasic pattern, observed at low cell density, has been reported recently on human prostate cancer cell lines treated with desmopressin, where low doses (1 nM) as well as a higher dose (1 µM) have an antiproliferative effect (41). This “biphasic effect” of peptides was shown some decades ago with OT on human uterus and oviduct (42).…”

Section: Discussionsupporting

confidence: 56%

Antiproliferative Effects of Oxytocin and Desmopressin on Canine Mammary Cancer Cells

et al. 2016

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Neoplasms of the mammary gland represent the most frequent tumor type in the female dog, and according to the histologic criteria, approximately 50% of them are malignant. In the most aggressive cases of mammary cancer, surgery is not enough to warrant a favorable outcome, and adjuvant therapies are needed to improve the patient’s overall survival. The aim of the present study was to evaluate the effects of two peptides on proliferation of a canine mammary cancer cell line derived from a simple carcinoma. The cell line CMT-U27 was grown in 96-well plates, at two cell densities (4 × 103 and 8 × 103 cells/well). Cultures were treated with oxytocin (OT) or desmopressin at five concentrations (10, 50, 100, 500, and 1000 nM). After 72 h of incubation, cell proliferation was determined by the MTT assay. Results showed that with 4 × 103 cells/well, OT at 50, 500, and 1000 nM was growth inhibitory for the cells, being statistically significant at 1000 nM. On the contrary, no antiproliferative effect was observed with 10 or 100 nM. At 8 × 103 cells/well, OT showed a significant antiproliferative effect only with the highest concentration (1000 nM). Desmopressin at 4 × 103 cells/well decreased cell viability at concentrations of 50, 100, 500, and 1000 nM (statistically significant with the highest concentration), while no effect was observed with 10 nM. With 8 × 103 cells/well, this peptide reduced cell growth at 100, 500, and 1000 nM. In conclusion, we suggest that these peptides may be potential and promising compounds for the treatment of dogs with simple carcinomas of the mammary gland. In vivo studies are required to confirm this hypothesis.

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Section: Discussionsupporting

confidence: 56%

Antiproliferative Effects of Oxytocin and Desmopressin on Canine Mammary Cancer Cells

et al. 2016

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“…Cell proliferation was assessed using the MTS assay as previously described . Cells were plated in 96‐well plates at a density of 4000 cells per well.…”

Section: Materials and Methodologymentioning

confidence: 99%

“…Cell proliferation was assessed using the MTS assay as previously described. 8,9 Cells were plated in 96-well plates at a density of 4000 cells per well. Cells were left to adhere for 24 h and dose standardization was performed using WIN ranging from 1 to 30 μM.…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Cannabinoid WIN 55,212‐2 induces cell cycle arrest and apoptosis, and inhibits proliferation, migration, invasion, and tumor growth in prostate cancer in a cannabinoid‐receptor 2 dependent manner

Roberto¹,

Klotz²,

Venkateswaran³

2018

The Prostate

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Background Cannabinoids have demonstrated anticarcinogenic properties in a variety of malignancies, including in prostate cancer. In the present study, we explored the anti‐cancer effects of the synthetic cannabinoid WIN 55,212‐2 (WIN) in prostate cancer. Methods Established prostate cancer cells (PC3, DU145, LNCaP) were treated with varying concentrations of WIN. Cell proliferation was determined by the MTS assay. The anti‐migration and anti‐invasive potential of WIN was examined by the wound healing assay and the matrigel invasion assay. Cell cycle analysis was performed by flow cytometry, and mechanistic studies were performed by Western blot. Athymic mice (n = 10) were inoculated with human PC3 cells. Once tumors reached 100 mm3, animals were randomized into two groups: saline control and WIN (5 mg/kg), delivered by intraperitoneal injection three times per week for 3 weeks. Results WIN significantly reduced prostate cancer cell proliferation, migration, invasion, induced apoptosis, and arrested cells in Go/G1 phase in a dose‐dependent manner. Mechanistic studies revealed these effects were mediated through a pathway involving cell cycle regulators p27, Cdk4, and pRb. Pre‐treatment with a CB2 antagonist, AM630, followed by treatment with WIN resulted in a reversal of the anti‐proliferation and cell cycle arrest previously seen with WIN alone. In vivo, administration of WIN resulted in a reduction in the tumor growth rate compared to control (P < 0.05). Conclusions The following study provides evidence supporting the use of WIN as a novel therapeutic for prostate cancer.

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“…Research to improve Docetaxel antitumor effects is ongoing [4]. Previous studies published by our group demonstrated this combination to have an additive effect by inhibiting growth, migration and invasion when tested on PC3 and LNCaP prostate cancer cells [5].…”

Section: Introductionmentioning

confidence: 99%

Effect of Combination therapy of Desmopressin and Docetaxel on prostate cancer cell DU145 proliferation, migration and growth

Hoffman

Sasaki²,

Roberto³

et al. 2016

GJCT

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Background: This study was designed to assess the efficacy of the combination of Desmopressin and Docetaxel for prostate cancer. Desmopressin has been demonstrated to inhibit tumor progression and metastasis in in vitro and in vivo models of breast cancer. Docetaxel, an anti-mitotic chemotherapeutic agent, is widely used for the treatment of castration resistant prostate cancer. However, it is associated with adverse effects and eventual drug resistance. This is the first report on the effect of combining Desmopressin and Docetaxel in prostate cancer, both in vitro and in vivo. Methods: An established castrate resistant prostate cancer cell line DU145 was used. Cellular proliferation was determined using the MTS assay. The migratory inhibition potential of Desmopressin alone and in combination with Docetaxel was accessed using the wound healing assay. In vivo evaluation was performed on a prostate cancer xenograft model using athymic nude mouse. Treatment was administered bi- weekly and tumor volume were measured throughout the treatment period. Eventually, after a six-week treatment period, tumors were excised and measured.Â Â Results: A combination therapy of 1 ÂµM Desmopressin with 100nM Docetaxel resulted in dramatic inhibition of proliferation of DU145 cells 72 hours post treatment compared to either agent along (p < 0.05). Wound healing assay revealed inhibition of cellular migration as well (p<0.05). The use of a xenograft mouse model followed by treatment with 5 mg/kg Docetaxel intraperitoneally with concomitant 2 Âµg/ml/kg Desmopressin administered intravenously 30 minutes before administering chemotherapy and 24 hours after, resulted in a significant decrease in tumor volume (P<0.05), while not impacting body weight.Conclusions: Desmopressin significantly enhanced the anti-proliferative and inhibiting the migratory potential of Docetaxel. Combination treatment had no additional effect on mice weight or mortality. These studies could enhance the efficacy of Docetaxel- based chemotherapy treatment for castrate resistant prostate cancer.

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A combination of desmopressin and docetaxel inhibit cell proliferation and invasion mediated by urokinase-type plasminogen activator (uPA) in human prostate cancer cells

Cited by 24 publications

References 20 publications

Antiproliferative Effects of Oxytocin and Desmopressin on Canine Mammary Cancer Cells

Antiproliferative Effects of Oxytocin and Desmopressin on Canine Mammary Cancer Cells

Cannabinoid WIN 55,212‐2 induces cell cycle arrest and apoptosis, and inhibits proliferation, migration, invasion, and tumor growth in prostate cancer in a cannabinoid‐receptor 2 dependent manner

Effect of Combination therapy of Desmopressin and Docetaxel on prostate cancer cell DU145 proliferation, migration and growth

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