Skin cancer is everywhere. It's the most common type of cancer out there. Most of these cases are nonmelanoma skin cancers, like basal cell carcinoma and squamous cell carcinoma. Melanoma, though less frequent, is the deadliest form. It's responsible for most skin cancer deaths.

One of the key players in skin cancer development is prostaglandin. Specifically, prostaglandin E2 (PGE2). It's involved in inflammation, blood vessel formation, immune system suppression, and tumor growth. This all happens through the cyclooxygenase (COX)-PGE2 pathway. PGE2 works through something called E-prostanoid (EP) receptors. These receptors activate different pathways that help cancer cells grow, survive, and spread.

In melanoma, the COX-2-E2 axis is a big deal. It's linked to how tumors evade the immune system and grow. There are drugs like celecoxib that can reduce nonmelanoma skin cancer cases. But long-term use isn't great because of side effects. This is where EP receptor antagonists come in. They might offer a more targeted approach with fewer side effects.

New treatments are on the horizon. Combining therapies with immune checkpoint inhibitors shows promise. This could be a game-changer in treating and preventing skin cancers.

There's still a lot to learn. More research is needed to understand PGE2 signaling better. This could lead to more effective treatments. The goal is to target the COX-PGE2-receptor axis more precisely.

Think about this: skin cancer isn't just about sun exposure. It's a complex process involving many factors, including prostaglandins. Understanding these factors can help in developing better treatments and prevention strategies.

Skin Cancer: The Unseen Role of Prostaglandins

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