Anticancer Effect of Sargassum oligocystom Hydroalcoholic Extract Against SW742, HT-29, WiDr, and CT-26 Colorectal Cancer Cell Lines and Expression of P53 and APC Genes.

PURPOSE: Colorectal cancer (CRC) is the third most common cancer in the world, with enhancing morbidity and mortality each year. Due to the drug resistance against CRC, the use of novel compounds besides chemotherapy is required. Natural seafood contains large amounts of biologically active substances with new chemical structures and new medicinal activities. The aim of this study was to evaluate the effects of hydroalcoholic extract of Sargassum oligocystom algae on SW742, HT-29, WiDr, and CT-26 CRC cell lines, and to evaluate the expression of P53 and APC genes using quantitative real-time PCR (RT-qPCR). METHODS: The cytotoxicity of S. oligocystom hydroalcoholic extract was determined by MTT and trypan blue methods in six different concentrations including 0.1, 0.2, 0.5, 1, 2, and 4 mg/mL on various CRC cell lines and a control group. The expression of P53 and APC genes in exposure to 2 mg/mL of the extract was also evaluated using RT-qPCR. RESULTS: The LD50 and LD90 of S. oligocystom included 0.5-1 and > 2 mg/mL, respectively mostly affecting SW742 and CT-26 cells. In the trypan blue test, 90% viability and death of cells were observed at 0.1 and 4 mg/mL of extract, respectively. The 2 mg/mL was a safe cytotoxic concentration. A significant viability decrease was observed at concentrations ≥ 1 mg/mL (p < 0.001). Sargassum oligocystom extract at 2 mg/mL significantly increased the expression of APC ranging 1.98-2.2-fold (p < 0.001) but not P53 gene which ranged 0.5-0.68-fold (p = 0.323) after 24 h. CONCLUSION: These results indicated that the brown algae S. oligocystom extract had significant antitumor effects against the SW742, HT-29, WiDr, and CT-26 CRC cell lines and especially CT-26, suggesting that it may be a potential candidate for further studies and therefore designing drugs of natural anticancer origin. The S. oligocystom had an anticancer effect via an increase in the APC gene expression.