The effects of phenoxodiol on the cell cycle of prostate cancer cell lines

Mahoney, Simon; Arfuso, Frank; Millward, Michael

doi:10.1186/s12935-014-0110-z

Cited by 15 publications

(10 citation statements)

References 31 publications

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“…These findings suggest that FAM46B regulates PC cell cycle progression and cell proliferation through the modulation of C-myc and Cyclin D1 expression. These data were in agreement with our findings on the roles of Cyclin D1 and C-myc in PC cell proliferation and cell cycle progression 34 , 35 . However, downregulation of C-myc and Cyclin D1 expression in PC-3 cells was associated with S and G2/M phase arrest rather than G0/G1 phase arrest 36 .…”

Section: Discussionsupporting

confidence: 93%

FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

Tao

Liu

et al. 2018

Exp Mol Med

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FAM46B is a member of the family with sequence similarity 46. Little is known about the expression and functional role(s) of FAM46B in prostate cancer (PC). In this study, the expression of FAM46B expression in The Cancer Genome Atlas, GSE55945, and an independent hospital database was measured by bioinformatics and real-time PCR analysis. After PC cells were transfected with siRNA or a recombinant vector in the absence or presence of a β-catenin signaling inhibitor (XAV-939), the expression levels of FAM46B, C-myc, Cyclin D1, and β-catenin were measured by western blot and real-time PCR. Cell cycle progression and cell proliferation were measured by flow cytometry and the CCK-8 assay. The effects of FAM46B on tumor growth and protein expression in nude mice with PC tumor xenografts were also measured. Our results showed that FAM46B was downregulated but that β-catenin was upregulated in patients with PC. FAM46B silencing promoted cell proliferation and cell cycle progression in PC, which were abrogated by XAV-939. Moreover, FAM46B overexpression inhibited PC cell cycle progression and cell proliferation in vitro and tumor growth in vivo. FAM46B silencing promoted β-catenin protein expression through the inhibition of β-catenin ubiquitination. Our data clearly show that FAM46B inhibits cell proliferation and cell cycle progression in PC through ubiquitination of β-catenin.

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Section: Discussionsupporting

confidence: 93%

FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

Tao

Liu

et al. 2018

Exp Mol Med

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“…We hypothesised that combining a tumour-specific radiation sensitiser with LuPSMA-617 would reduce radiation resistance, prolonging and deepening treatment responses compared with LuPSMA-617 alone. We proposed that idronoxil, via its effects on apoptosis, cell cycle arrest, and topoisomerase II, may impair DNA repair mechanisms and improve sensitivity to LuPSMA-617 [9,10,26]. Furthermore, we postulated 9) 0 (0) 11 (34) Pneumonitis a 0 (0) 1 ( 3) 0 (0) 1 (3) Neutropenia 3 ( 9) 0 (0) 0 (0) 3 ( 9) AE = adverse event.…”

Section: Discussionmentioning

confidence: 99%

Phase I/II Trial of the Combination of 177Lutetium Prostate specific Membrane Antigen 617 and Idronoxil (NOX66) in Men with End-stage Metastatic Castration-resistant Prostate Cancer (LuPIN)

Crumbaker

Pathmanandavel

Yam

et al. 2021

European Urology Oncology

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Background: Trials of lutetium prostate specific membrane antigen (PSMA) in men with metastatic castration-resistant prostate cancer (mCRPC) have demonstrated good safety and efficacy, but combination strategies may improve outcomes. Idronoxil is a synthetic flavonoid derivative with radiosensitising properties. Objective: To evaluate the safety and activity of 177 Lu PSMA 617 (LuPSMA-617) in combination with idronoxil suppositories (NOX66) in patients with end-stage mCRPC. Design, setting, and participants: Thirty-two men with progressive mCRPC previously treated with taxane-based chemotherapy (91% treated with both docetaxel and cabazitaxel) and abiraterone and/or enzalutamide were enrolled in this phase I dose escalation study with phase II dose expansion. Intervention: Screening with 68 Ga PSMA and 18 F-fludeoxyglucose positron emission tomography (PET)/computed tomography (CT) was performed. Men received up to six cycles of LuPSMA-617 (7.5 GBq) on day 1, with escalating doses of NOX66 on days 1-10 of a 6-wk cycle. Cohort 1 (n = 8) received 400 mg and cohort 2 (n = 24) 800 mg of NOX66. Outcome measurements and statistical analysis: Adverse events (AEs), pain inventory scores, prostate-specific antigen (PSA) response, progression-free survival, and overall survival were evaluated. Results and limitations: Fifty-six men were screened and 32 (57%) were enrolled with a screen failure rate of 21% for PET imaging criteria. Dosing was as follows: 97% (31/32) received two or more doses and 47% (15/32) completed six doses. Common

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“…The relative gene expression was calculated using 2 −ΔΔC T method,9 where ΔΔC T values of each sample were calculated from C T values; ΔΔC T = [C T target gene–C T GAPDH ] (treated sample) –[C T target gene–C T GAPDH ] (untreated sample) . The primers used in the experiments were as follows:10,11 Bax : F, 5′-GCTGGACATTGGACTTCCTC-3′ and R, 5′-TCAGCCCATCTTCTTCCAGA-3′; Bcl-2 : F, 5′-TGTGGATGACTGAGTACCTGAACC-3′ and R, 5′-CAGCCAGGAGAAATCAAACAGAG-3′; GAPDH (housekeeping gene): F, 5′-CGTCTGCCCTATCAACTTTCG-3′ and R, 5′-CGTTTCTCAGGCTCCCTCT-3′. The primers were synthesized by LGC Biosearch technologies (Novato, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Anti-proliferative Effects ofAndroctonus amoreuxiScorpion andCerastes cerastesSnake Venoms on Human Prostate Cancer Cells

et al. 2017

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The present study evaluated the effects of Androctonus amoreuxi scorpion venom, Cerastes cerastes snake venom and their mixture on prostate cancer cells (PC3). An MTT assay was used to determine the anti-proliferative effect of the venoms, while quantitative real time PCR was used to evaluate the expression of apoptosis-related genes (Bax and Bcl-2). Furthermore, colorimetric assays were used to measure the levels of malondialdehyde (MDA) and antioxidant enzymes. Our results show that the venoms significantly reduced PC3 cell viability in a dose-dependent manner. On the other hand, these venoms significantly decreased Bcl-2 gene expression. Additionally, C. cerastes venom significantly reduced Bax gene expression, while A. amoreuxi venom and a mixture of A. amoreuxi & C. cerastes venoms did not alter Bax expression. Consequently, these venoms significantly increased the Bax/Bcl-2 ratio and the oxidative stress biomarker MDA. Furthermore, these venoms also increased the activity levels of the antioxidant enzymes, catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase. Overall, the venoms have cytotoxic and anti-proliferative effects on PC3 cells.

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The effects of phenoxodiol on the cell cycle of prostate cancer cell lines

Cited by 15 publications

References 31 publications

FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

Phase I/II Trial of the Combination of 177Lutetium Prostate specific Membrane Antigen 617 and Idronoxil (NOX66) in Men with End-stage Metastatic Castration-resistant Prostate Cancer (LuPIN)

Anti-proliferative Effects ofAndroctonus amoreuxiScorpion andCerastes cerastesSnake Venoms on Human Prostate Cancer Cells

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