Prospects of NSAIDs administration as double-edged agents against endometrial cancer and pathological species of the uterine microbiome.
Olga KuźmyczPaweł StączekPublished in: Cancer biology & therapy (2020)
Many types of cancers, including endometrial cancer, were found to have cyclooxygenase-2 (COX-2) overexpression. Because this enzyme belongs to the group of pro-inflammatory enzymes, so-called NSAIDs (non-steroidal anti-inflammatory drugs) directly inhibit its activity. An increasing number of reports on COX-2 involvement in cancer, as well as on the role of microbiota in abnormal metabolism and signaling of cells, forces the development of new NSAID types. Besides, NSAIDs can affect some bacteria, which are vaginal/endometrial microbiome members. The overgrowth of those species was found to be a major cause of some uterus diseases. Those infections can lead to chronic inflammatory response and suppress anti-tumorigenic cell pathways. The purpose of this review is to highlight the COX-2 enzyme role in endometrial cancer, the potential effect of the endometrial microbiome on COX-2 enzyme overexpression, and the prospects of NSAIDs use in terms of this type of cancer.
Keyphrases
- endometrial cancer
- anti inflammatory drugs
- papillary thyroid
- inflammatory response
- cell proliferation
- squamous cell
- induced apoptosis
- transcription factor
- current status
- cell therapy
- stem cells
- squamous cell carcinoma
- toll like receptor
- lipopolysaccharide induced
- signaling pathway
- lps induced
- mesenchymal stem cells
- nitric oxide synthase
- climate change