Astaxanthin promotes apoptosis by suppressing growth signaling pathways in HT-29 colorectal cancer cells.

Colorectal cancer (CRC) is the third most frequently diagnosed malignancy globally and ranks second in cancer-related mortality. Despite advancements in therapeutic approaches, the need for novel, effective and less toxic treatment strategies remains critical. Astaxanthin (ATX), a naturally occurring xanthophyll carotenoid, has attracted attention due to its strong antioxidant, anti-inflammatory and anti-cancer properties. This study aimed to evaluate the antiproliferative and pro-apoptotic effects of ATX on CRC through its influence on key molecular pathways, involved in tumorigenesis. The human colorectal adenocarcinoma cell line HT-29 was treated with varying concentrations of ATX (10 µM and 20 µM) for 24 h. Cell viability was assessed using the XTT assay. The expression levels of HER2, EGFR, ERK1, ERK2 and mTOR were quantified via enzyme-linked immunosorbent assay (ELISA). Immunofluorescence staining was used to evaluate the expression of EGFR and caspase-3 proteins. ATX exhibited significant antiproliferative and pro-apoptotic effects on HT-29 cells, with an IC50 value of 10.98 µM at 24 h. Treatment with ATX (10.98 µM) led to a marked increase in caspase-3 expression and a significant reduction in EGFR levels. Additionally, HER2, ERK1 and ERK2 levels were significantly downregulated, while mTOR expression remained unaffected. Flow cytometry analysis revealed a significant increase in apoptotic cell populations following ATX treatment, compared to the control group. ATX exerts notable antiproliferative and pro-apoptotic effects on CRC cells, potentially through modulation of the EGFR/HER2/ERK signaling pathway. These findings suggest that ATX may serve as a promising candidate for further investigation as an adjunctive or standalone therapeutic agent in the treatment of CRC.