Abstract
ABSTRACTMeclofenamic acid is a nonsteroidal anti-inflammatory drug that has shown therapeutic potential for different types of cancers, including androgen-independent prostate neoplasms. The antitumor effect of diverse nonsteroidal anti-inflammatory drugs has been shown to be accompanied by histological and molecular changes that are responsible for this beneficial effect. The objective of the present work was to analyze the histological changes caused by meclofenamic acid in androgen-independent prostate cancer. Tumors were created in a nude mouse model using PC3 cancerous human cells. Meclofenamic acid (10 mg/kg/day; experimental group, n=5) or saline solution (control group, n=5) was administered intraperitoneally for twenty days. Histological analysis was then carried out on the tumors, describing changes in the cellular architecture, fibrosis, and quantification of cellular proliferation and tumor vasculature. Meclofenamic acid causes histological changes that indicate less tumor aggression (less hypercellularity, fewer atypical mitoses, and fewer nuclear polymorphisms), an increase in fibrosis, and reduced cellular proliferation and tumor vascularity. Further studies are needed to evaluate the molecular changes that cause the beneficial and therapeutic effects of meclofenamic acid in androgen-independent prostate cancer.
Highlights
Prostate cancer (PCa) is a worldwide public health problem and is the first cause of death by cancer in men over fifty years of age [1]
Tumors treated with PBS had greater hypercellularity, greater nuclear polymorphism, and a greater number of atypical mitoses than the tumors treated with meclofenamic acid (Figure-1)
Treatment with meclofenamic acid produces significant histological changes that can be considered beneficial and they are concordant with antitumor effects previously reported for this drug
Summary
Prostate cancer (PCa) is a worldwide public health problem and is the first cause of death by cancer in men over fifty years of age [1]. The growth of this neoplasia is generally dependent on androgen stimulation, at a given moment it can proliferate in a hormone-independent manner. The inhibition processes of both COX and AKR1C are involved in the NSAID antitumor effect, and fenamates show great potential in the treatment of cancer [8, 9]
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