Cancer research largely focuses on the epithelial-to-mesenchymal transition (EMT) as a critical mechanism required for the acquisition of the invasive potential of cancer cells, which can culminate in the formation of metastases. This process involves the transformation of epithelial cells into mesenchymal cells by acquiring suppressed levels of E-cadherin, an anti-EMT marker with a role in the establishment of intercellular junctions. Also, the expression of pro-EMT markers, such as the regulatory marker SNAIL, as well as the effectors N-cadherin and Vimentin, rises as cancer advances. Therefore, there is an emerging need for bioactive substances able to target and modulate EMT markers and reverse this process. The unsaturated fatty acid 10H2DA has not been investigated so far regarding its potential to target specific EMT markers in colorectal cancer (CRC), which was the aim of this study.

Colorectal cancer cell line SW-480 isolated from stage II CRC was treated with 10H2DA in two selected concentrations of 10 and 100 μM. After 24 h, the gene expression of E-cadherin, SNAIL, N-cadherin, and Vimentin markers was assessed by the qPCR method. Additionally, changes in the protein concentration of these markers between control (untreated) and treated cells were evaluated by immunofluorescent assay.

Queen bee acid successfully upregulated the expression of the anti-EMT marker E-cadherin. Our results also point towards a downregulated expression of the pro-EMT regulatory marker SNAIL, as well as the effector markers N-cadherin and Vimentin. This successively led to a significant elevation in E-cadherin on the protein level, and also to an inhibition of pro-EMT proteins, namely, SNAIL, N-cadherin, and Vimentin.

The potential of the unsaturated acid 10H2DA to modulate the expression of specific and significant EMT markers in CRC is obvious and prominent, and it should not be neglected in future studies regarding anticancer therapeutic approaches.