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The molecular targets of diclofenac differs from ibuprofen to induce apoptosis and epithelial mesenchymal transition due to alternation on oxidative stress management p53 independently in PC3 prostate cancer cells.

ABSTRACT: Background:Prostate cancer is the most common type of cancer among men. Studies showed that the regular use of nonsteroidal antiinflammatory drugs might reduce disease progression risk for prostate cancer patients with prostate cancer. We evaluated the effects of ectopic expression of p53 on the biological functions of ibuprofen and diclofenac. Materials and methods:For this purpose, We investigated cell death decision pathways related to survival and aggressive cellular phenotypes such as extrinsic/intrinsic apoptosis decision, Protein Kinase B/ Forkhead box O (AKT/FoxO) axis, mitogen-activated protein kinases (MAPKs), reactive oxygen species (ROS) generation, and EMT (epithelial mesenchymal transition) in wild type and p53 + PC3 prostate cancer cells. Results and Conclusions:Ibuprofen (1 mM) and diclofenac (250 ?M) effectively induced cell cycle arrest and led to apoptosis via modulating both extrinsic and intrinsic pathways. However, diclofenac was the only drug to generate ROS intermediates. Diclofenac triggered a typical EMT process with downregulated E-cadherin and upregulated N-cadherin, vimentin, and Snail in PC3 cells, regardless of p53 expression. In conclusion, although both drugs are effective on cell death mechanism, only diclofenac caused EMT because of increased ROS generation independent of p53. On the other hand, ibuprofen could inhibit metastasis via upregulating E-cadherin. The biological targets of both nonsteroidal antiinflammatory drugs are different to highlight their role in cell survival and death axis.

SUBMITTER: Arisan ED

PROVIDER: S-EPMC6962753 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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The molecular targets of diclofenac differs from ibuprofen to induce apoptosis and epithelial mesenchymal transition due to alternation on oxidative stress management p53 independently in PC3 prostate cancer cells.

Arisan Elif D ED Akar Remzi O RO Rencuzogullari Ozge O Obakan Yerlikaya Pinar P Coker Gurkan Ajda A Akın Beyza B Dener Elif E Kayhan Ecem E Palavan Unsal Narcin N

Prostate international 20191114 4

<h4>Background</h4>Prostate cancer is the most common type of cancer among men. Studies showed that the regular use of nonsteroidal antiinflammatory drugs might reduce disease progression risk for prostate cancer patients with prostate cancer. We evaluated the effects of ectopic expression of p53 on the biological functions of ibuprofen and diclofenac.<h4>Materials and methods</h4>For this purpose, We investigated cell death decision pathways related to survival and aggressive cellular phenotype ...[more]

PMID: 31970141

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Project description:Background: The presence of pharmaceuticals at low concentrations (ng to μg) in the environment has become a hot spot for researchers in the past decades due to the unknown environmental impact and the possible damages they might have to the plantae and fauna present in the aquatic systems, as well as to the other living organisms. Objectives: The aim of the present investigation was to develop a bacterial consortium isolated from different origins to evaluate the ability of such a consortium to remove a mixture of pharmaceuticals in the batch system at lab scale, as well as assessment of its resistance to the other micropollutants present in the environment. Material and Methods: Using a closed bottle test, biodegradation of the mixed pharmaceuticals including Diclofenac (DCF), Ibuprofen (IBU), and Sulfamethoxazole (SMX) (at a concentration of 3 mg.L-1 of each drug) by the bacterial consortium was investigated. The test was carried out under metabolic (pharmaceutical was used as the sole source of carbon) and co-metabolic condition (in the presence of glucose). Finally, the ability of the bacterial consortium to resist other micropollutants like antibiotics and heavy metals was investigated. Results: Under the metabolic condition, the mixed bacteria (i.e., consortium) were able to metabolize 23.08% and 9.12% of IBU, and DCF at a concentration of 3 mg.L-1 of each drug, respectively. Whereas, in co-metabolic conditions, IBU was eliminated totally, in addition, 56% of the total concentration of DCF was removed, as well. In both metabolic and cometabolic conditions, removal of SMX was not observed. The selected bacteria were able to resist to most of the applied antibiotics and the used heavy metals, except mercury, where only one strain (S4) was resistant to the later heavy metal. Conclusion: Results suggest that the developed consortium might be an excellent candidate for the application in the bioremediation process for treating ecosystems contaminated with the pharmaceutical.

Dataset Information

The molecular targets of diclofenac differs from ibuprofen to induce apoptosis and epithelial mesenchymal transition due to alternation on oxidative stress management p53 independently in PC3 prostate cancer cells.

Publications

The molecular targets of diclofenac differs from ibuprofen to induce apoptosis and epithelial mesenchymal transition due to alternation on oxidative stress management p53 independently in PC3 prostate cancer cells.

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