# The Evaluation of Potential Anticancer Activity of Meloxicam—In Vitro Study on Amelanotic and Melanotic Melanoma

## TL;DR

This study shows that meloxicam, an anti-inflammatory drug, can reduce the growth of melanoma cells by disrupting their function and causing cell death.

## Contribution

The study demonstrates meloxicam's anticancer effects on both amelanotic and melanotic melanoma cell lines, with amelanotic cells being more sensitive.

## Key findings

- Amelanotic C32 melanoma cells were more sensitive to meloxicam, showing reduced proliferation and disrupted redox balance.
- Meloxicam induced apoptosis and reduced mitochondrial potential in melanoma cells.
- The drug's effects were confirmed through multiple assays, including ROS levels and caspase activity.

## Abstract

Meloxicam (MLX), a member of the non-steroidal anti-inflammatory drugs (NSAIDs), is a preferential inhibitor of cyclooxygenase-2 (COX-2) responsible for the synthesis of pro-inflammatory prostaglandins. MLX, due to its inhibition of the COX-2 enzyme, which is overexpressed in many cancers, including melanoma, leading to rapid growth, angiogenesis, and metastasis, represents a potentially important compound with anticancer activity. This study aimed to investigate the potential anticancer activity of meloxicam against amelanotic C32 and melanotic COLO 829 melanoma cell lines. The objective was achieved by assessing cell metabolic activity using the WST-1 assay and analyzing mitochondrial potential, levels of reduced thiols, annexin, and caspases 3/7, 8, and 9 by imaging cytometry, as well as assessing reactive oxygen species (ROS) levels using the H2DCFDA probe. The amelanotic melanoma C32 was more sensitive to MLX exposure, thus exhibiting antiproliferative effects, a disruption of redox homeostasis, a reduction in mitochondrial potential, and an induction of apoptosis. The results provide robust molecular evidence supporting the pharmacological effects of MLX, highlighting its potential as a valuable agent for in vivo melanoma treatment.