Histological changes caused by meclofenamic acid in androgen independent prostate cancer tumors: evaluation in a mouse model

Delgado‐Enciso, Iván; Soriano-Hernández, Alejandro D.; Rodríguez-Hernández, Alejandrina; Galvan-Salazar, Hector R; Montes-Galindo, Daniel A.; Martínez-Martínez, Rafael; Valdez-Velázquez, Laura Leticia; González-Álvarez, Rafael; Espinoza‐Gómez, Francisco; Newton-Sánchez, Óscar Alberto; Lara-Esqueda, Agustín; Guzmán-Esquivel, José

doi:10.1590/s1677-5538.ibju.2013.00186

Cited by 8 publications

(7 citation statements)

References 30 publications

(28 reference statements)

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“…In addition, other COX enzyme inhibitors such as Ibuprofen and celecoxib did not affect IL-1β release (Daniels et al, 2016). These fenamic acid derivatives have been studied in a variety of disease models including AD, prostate cancer, and more (Delgado-Enciso et al, 2015;Mangan et al, 2018).…”

Section: Fenamic Acidsmentioning

confidence: 99%

The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases

Blevins

Biby

et al. 2022

Front. Aging Neurosci.

165

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The NLRP3 inflammasome is a multiprotein complex that plays a pivotal role in regulating the innate immune system and inflammatory signaling. Upon activation by PAMPs and DAMPs, NLRP3 oligomerizes and activates caspase-1 which initiates the processing and release of pro-inflammatory cytokines IL-1β and IL-18. NLRP3 is the most extensively studied inflammasome to date due to its array of activators and aberrant activation in several inflammatory diseases. Studies using small molecules and biologics targeting the NLRP3 inflammasome pathway have shown positive outcomes in treating various disease pathologies by blocking chronic inflammation. In this review, we discuss the recent advances in understanding the NLRP3 mechanism, its role in disease pathology, and provide a broad review of therapeutics discovered to target the NLRP3 pathway and their challenges.

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Section: Fenamic Acidsmentioning

confidence: 99%

The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases

Blevins

Biby

et al. 2022

Front. Aging Neurosci.

165

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“…Recent studies demonstrated that targeting the phosphatidylinositide 3-kinase (PI3K)/AKT signaling pathway is a major strategy for treating androgen-independent PCa [74] or alternately meclofenamic acid can be prescribed. Meclofenamic acid is a nonsteroidal anti-inflammatory drug that has shown therapeutic potential for different types of cancers, including androgen-independent PCa [75]. The time point for intervention application was suggested to be at the point when the level of prostate-specific antigen retrogrades.…”

Section: Bioenergetic Profile Of Rmcs Affected By Bicmentioning

confidence: 99%

Bicalutamide Elicits Renal Damage by Causing Mitochondrial Dysfunction via ROS Damage and Upregulation of HIF-1

Chen

et al. 2020

IJMS

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Combined androgen blockade using bicalutamide (Bic) is a therapeutic choice for treating prostate cancer (PCa). However, even at regular clinical dosages, Bic frequently shows adverse effects associated with cardiovascular and renal damage. Previously, we found that Bic selectively damaged mesangial cells compared to tubular cells and in an in vivo rat model, we also found renal damage caused by Bic. In the present study, a rat mesangial cell model was used to further the investigation. Results indicated that Bic enhanced lactate dehydrogenase release, reactive oxygen species (ROS) production, lysosome population and kidney injury molecule-1 and decreased N-cadherin. Bic elicited mitochondrial swelling and reduced the mitochondrial potential, resulting in severe suppression of the oxygen consumption rate (OCR), maximum respiration and ATP production. The hypoxia-inducible factor (HIF)-1 transcriptional activity and messenger RNA were significantly upregulated in dose-dependent manners. The HIF-1 protein reached a peak value at 24 h then rapidly decayed. BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 and cleaved caspase-3 were dose-dependently upregulated by Bic (60 M) and that eventually led to cell apoptosis. It is suggested that Bic induces renal damage via ROS and modulates HIF-1 pathway and clinically, some protective agents like antioxidants are recommended for co-treatment.

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“…Meclofenamic acid (MA), an NSAID, has been shown to have anti-carcinogenic effects on various types of cancer. [9][10][11]20 However, the effect of the drug on LNCaP cell migration and invasion has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…8 Meclofenamic acid (MA), a nonsteroidal antiinflammatory drug (NSAID), has been shown to have anticarcinogenic effects in addition to its anti-inflammatory properties. [9][10][11][12][13] It has been shown that MA inhibited the growth of several cancer types including uterine cervical cancer and bladder cancer. However, it was realized that there is no study investigating the role of MA on androgen-dependent PC.…”

Section: Introductionmentioning

confidence: 99%

Meclofenamic acid inhibits the invasion and migration of LNCaP prostate carcinoma cells by regulating vimentin expression

KANLI,

YANAR

2022

Acta Med Nicomedia

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Objectives: Despite various studies to improve the early detection and development of novel treatment agents, no significant progress has been made in the treatment of prostate cancer. Moreover, the metastasis of prostate carcinoma is a major challenge in treatment modalities. Therefore, in the present study, it was aimed to investigate the effect of meclofenamic acid (MA), a nonsteroidal anti-inflammatory drug, on the migration and invasion of LNCaP prostate carcinoma cells. Methods: Firstly, the non-toxic concentrations of MA on LNCaP cells were determined by trypan blue exclusion assay. After that, the effect of MA on migration and invasion was assessed by wound healing assay and matrigel invasion assay, respectively. Finally, the expression level of vimentin, which is a marker for epithelial-to-mesenchymal cell transition, was assessed by western blotting. Results: The results of trypan blue exclusion assay showed that 60 and 80 µM concentrations of MA were non-toxic to the cells. The migration rate of non-treated control cells was 44.4%, while it was significantly reduced to 12.9% and 2.9% in 60 and 80 µM MA-treated groups, respectively. When the cells were treated with 80 µM MA, the drug significantly reduced the invasion of LNCaP cells from 52% to 30.3%. Western blot results showed that the level of vimentin expression was significantly decreased in MA-treated cells. Conclusion: The study shows for the first time that MA inhibits the invasion and migration of prostate cancer LNCaP cells by decreasing the expression level of vimentin.

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Histological changes caused by meclofenamic acid in androgen independent prostate cancer tumors: evaluation in a mouse model

Cited by 8 publications

References 30 publications

The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases

The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases

Bicalutamide Elicits Renal Damage by Causing Mitochondrial Dysfunction via ROS Damage and Upregulation of HIF-1

Meclofenamic acid inhibits the invasion and migration of LNCaP prostate carcinoma cells by regulating vimentin expression

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