Antitumor effect of meclofenamic acid on human androgen-independent prostate cancer: a preclinical evaluation

Soriano-Hernández, Alejandro D.; Galvan-Salazar, Hector R; Montes-Galindo, Daniel A.; Rodríguez-Hernández, Alejandrina; Martínez-Martínez, Rafael; Guzmán-Esquivel, José; Valdez-Velázquez, Laura Leticia; Baltazar-Rodríguez, Luz M.; Espinoza‐Gómez, Francisco; Rojas-Martínez, Augusto; Ortíz-López, Rocío; González-Álvarez, Rafael; Delgado‐Enciso, Iván

doi:10.1007/s11255-011-0012-0

Cited by 31 publications

(20 citation statements)

References 28 publications

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“…This fact is in agreement with the suggested proposal that this meclofenamic acid may have stronger activity in neoplasias with a glandular origin (11). Nonetheless, the results of the present study showed the antineoplastic action in human cells of a squamous nature (SiHa, HPV-16 + ).…”

Section: Discussionsupporting

confidence: 94%

“…Notably, the drugs used in the present study (NSAIDs and dexamethasone) exhibited varied antineoplastic effects, which confirms that the inhibition of inflammation is not enough to generate an effect against cancer. The antitumor activity of meclofenamic acid was recently reported in prostate cancer (11). It was proposed that the effect is not only caused by COX-2 inhibition, but also by the strong inhibition of AKRs.…”

Section: Discussionmentioning

confidence: 99%

“…The exerted inhibition of the NSAIDs over these enzymes has been considered as a proposed mechanism of the antineoplastic effect (10). Several anti-inflammatories have also been probed experimentally as a UCC treatment, however, the obtained results were varied and it is difficult to establish the substance that has the greatest antineoplastic effect (11). In spite of the fact that meclofenamic acid has previously been proposed as a promising antineoplastic drug, the fenamates have not yet been investigated in UCC.…”

Section: Introductionmentioning

confidence: 99%

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Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

et al. 2015

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Abstract. Uterine cervical cancer (UCC) is one of the main causes of cancer-associated mortality in women. Inflammation has been identified as an important component of this neoplasia; in this context, anti-inflammatory drugs represent possible prophylactic and/or therapeutic alternatives that require further investigation. Anti-inflammatory drugs are common and each one may exhibit a different antineoplastic effect. As a result, the present study investigated different anti-inflammatory models of UCC in vitro and in vivo. Celecoxib, sulindac, nimesulide, dexamethasone, meclofenamic acid, flufenamic acid and mefenamic acid were tested in UCC HeLa, VIPA, INBL and SiHa cell lines. The cytotoxicity of the drugs was evaluated in vitro. Celecoxib, sulindac, nimesulide, mefenamic acid and flufenamic acid presented with slight to moderate toxicity (10-40% of cell death corresponding to 100 µM) in certain cell lines, while meclofenamic acid exhibited significant cytotoxicity in all essayed cell lines (50-90% of cell death corresponding to 100 µM). The meclofenamic acid was tested in murine models (immunodeficient and immunocompetent) of UCC, which manifested a significant reduction in tumor growth and increased mouse survival. It was demonstrated that of the evaluated anti-inflammatory drugs, meclofenamic acid was the most cytotoxic, with a significant antitumor effect in murine models. Subsequent studies are necessary to evaluate the clinical utility of this drug.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

et al. 2015

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“…Preclinical in vitro and in vivo (xenograft nude mouse model) studies in PCa have demonstrated that the fenamate NSAIDs have a more notable antineoplastic effect compared with previously examined NSAIDs in PCa (31). Mefenamic acid and meclofenamate demonstrate this type of antitumor effect (31). Notably, in a preclinical study, mefenamic acid, a freely sold NSAID whose everyday use is for dysmenorrhea, had a cytotoxic effect on PCa cells at concentrations that can be feasibly achieved in human plasma (31).…”

Section: Decreased Biochemical Progression In Patients With Castratiomentioning

confidence: 99%

Section: Decreased Biochemical Progression In Patients With Castratiomentioning

confidence: 99%

Decreased biochemical progression in patients with castration‑resistant prostate cancer using a novel mefenamic acid anti‑inflammatory therapy: A randomized controlled trial

et al. 2020

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Prostate cancer (PCa) is the second most common non-dermatological cancer in men and is a growing public health problem. Castration-resistant disease (CRD) is the most advanced stage of the disease and is difficult to control. Patients with CRD may no longer accept conventional therapies as they are not in appropriate clinical conditions or they refuse to receive it. Given that inflammation is an essential component of CRD origin and progression, anti-inflammatory agents could be a therapeutic option with fenamates as one of the proposed choices. A prospective, randomized, double-blinded, 2-arm, parallel group, phase II-III clinical trial was performed involving 20 patients with CRD-PCa (with a prostate specific antigen level <100 ng/ml) that were undergoing androgen deprivation therapy (ADT) and did not accept any established treatment for that disease stage. In addition to ADT, 10 patients received placebo and 10 received mefenamic acid (500 mg orally every 12 h) for 6 months. The primary endpoint was the change in serum prostate-specific antigen (PSA) at 6 months. The PSA levels decreased significantly with mefenamic acid (an average 42% decrease), whereas there was an average 55% increase in the placebo group (P=0.024). In the patients treated with the placebo, 70% had biochemical disease progression (an increase of ≥25% in PSA levels), which did not occur in any of the patients treated with mefenamic acid (relative risk= 0.12; 95% confidence interval, 0.01-0.85; P= 0.033). There was a significant increase in quality of life (EQ-5D-5L score) and body mass index (BMI) with the experimental treatment. In conclusion, mefenamic acid administration decreased biochemical progression in patients with castration resistant PCa, improved their quality of life and increased their BMI. Future studies are required in order to strengthen the findings of the present clinical trial. Trial registration, Cuban Public Registry of Clinical Trials Database RPCEC00000248,

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Interplay between m⁶A epitranscriptome and epigenome in cancer: current knowledge and therapeutic perspectives

Bove

Amin

Babaei

et al. 2022

Intl Journal of Cancer

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Chromatin has an extremely flexible structure that allows the fine regulation of gene expression. To orchestrate this process, small chemical modifications are dynamically added or removed on DNA, RNA and histone substrates. Epigenetic modifications govern a plethora of key cellular functions, whose dysregulation contributes to oncogenesis. The interrelationship between (irreversible) genetic mutations and (reversible) epigenetic alterations and how this crosstalk regulates gene expression has long been a major area of interest. Marks modulating the RNA code (epitranscriptome), such as the well-studied N 6 -methyladenosine (m 6 A), are known to influence stability, metabolism and life cycle of many mRNAs, including cancer-associated transcripts.Together, epigenetic and epitranscriptomic pathways therefore control the entire cellular expression profile and, eventually, cell fate. Recently, previously undescribed crosstalk between these two pathways has started to be unrevealed. For example, m 6 A and its effectors cooperate with histone modifications to localize chromatinmodifying complexes to their target regions. Epigenetic marks governing the expression of m 6 A factors can also be found at specific genetic loci. m 6 A itself can mark noncoding RNAs (including lncRNAs, circRNAs and miRNAs), influencing their structure, maturation and function. These interactions affect both cell physiology and pathology. Clear evidence that dysregulation of this network plays a role in cancer has emerged, suggesting a new layer of complexity in the landscape of gene expression. Here, we summarize current knowledge on the interplay between m 6 A

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Antitumor effect of meclofenamic acid on human androgen-independent prostate cancer: a preclinical evaluation

Abstract: Meclofenamic acid was shown to be a potential antineoplastic agent for both androgen-dependent and androgen-independent prostate cancer.

Cited by 31 publications

References 28 publications

Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

Decreased biochemical progression in patients with castration‑resistant prostate cancer using a novel mefenamic acid anti‑inflammatory therapy: A randomized controlled trial

Interplay between m⁶A epitranscriptome and epigenome in cancer: current knowledge and therapeutic perspectives

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Antitumor effect of meclofenamic acid on human androgen-independent prostate cancer: a preclinical evaluation

Abstract: Meclofenamic acid was shown to be a potential antineoplastic agent for both androgen-dependent and androgen-independent prostate cancer.

Cited by 31 publications

References 28 publications

Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

Anti-inflammatory drugs and uterine cervical cancer cells: Antineoplastic effect of meclofenamic acid

Decreased biochemical progression in patients with castration‑resistant prostate cancer using a novel mefenamic acid anti‑inflammatory therapy: A randomized controlled trial

Interplay between m6A epitranscriptome and epigenome in cancer: current knowledge and therapeutic perspectives

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Interplay between m⁶A epitranscriptome and epigenome in cancer: current knowledge and therapeutic perspectives