Abstract
The prostaglandins constitute a family of lipids of 20 carbon atoms that derive from polyunsaturated fatty acids such as arachidonic acid. Traditionally, prostaglandins have been linked to inflammation, female reproductive cycle, vasodilation, or bronchodilator/bronchoconstriction. Recent studies have highlighted the involvement of these lipids in cancer. In this review, existing information on the prostaglandins associated with different types of cancer and the advances related to the potential use of them in neoplasm therapies have been analyzed. We can conclude that the effect of prostaglandins depends on multiple factors, such as the target tissue, their plasma concentration, and the prostaglandin subtype, among others. Prostaglandin D2 (PGD2) seems to hinder tumor progression, while prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2α) seem to provide greater tumor progression and aggressiveness. However, more studies are needed to determine the role of prostaglandin I2 (PGI2) and prostaglandin J2 (PGJ2) in cancer due to the conflicting data obtained. On the other hand, the use of different NSAIDs (non-steroidal anti-inflammatory drugs), especially those selective of COX-2 (cyclooxygenase 2), could have a crucial role in the fight against different neoplasms, either as prophylaxis or as an adjuvant treatment. In addition, multiple targets, related to the action of prostaglandins on the intracellular signaling pathways that are involved in cancer, have been discovered. Thus, in depth research about the prostaglandins involved in different cancer and the different targets modulated by them, as well as their role in the tumor microenvironment and the immune response, is necessary to obtain better therapeutic tools to fight cancer.
Highlights
We have revised many published works with interesting data about prostaglandins that are involved in different types of cancer, and we have described some of the latest therapeutic advances to treat cancer by acting on prostaglandins and enzymes related to these neoplasms
One study performed with cell lines, human tissues and mouse models showed that upregulation of the co-activator CRTC1 stimulates expression of the COX-2 gene and the production of prostaglandin prostaglandin E2 (PGE2), which in turn leads to dephosphorylation and activation of CRTC1, closing the feedback loop that increases tumorigenicity of colorectal cancer [65]
Prostaglandins of the Prostaglandin D2 (PGD2) type are clearly related to better survival expectations, since they can hinder tumor progression
Summary
C. Lieb demonstrated that the uterine endometrium contracted and relaxed rhythmically after exposure to semen [1]. In 1939, Ulf von Euler stated that this contraction was due to the action of an unknown unsaturated lipid, which he called prostaglandin [2]. Bergstrom observed the effects of the administration of prostaglandin E in humans [3]. A. van Dorp reported having achieved the synthesis of PGE2 from arachidonic acid and to have discovered the crystalline structure of PGF2α and PGE2, which allowed the synthesis of prostaglandins in sufficient quantities to carry out pharmacological studies [4]. R. Vane demonstrated that ASA (acetyl salicylic acid, aspirin) and non-steroidal anti-inflammatory agents inhibited the synthesis of prostaglandins [5]. Vane, received the Nobel Prize in Medicine and Physiology in 1982
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