EACR25-0432

Sesamin inhibits human colorectal cancer HCT-116 cell growth by inducing apoptosis

Y. Chen¹, Y. Huang¹, C. Wu², Y. Chen³, Y. Wu⁴, S. Hsieh¹

¹National Kaohsiung University of Science and Technology, Department of Seafood Science, Kaohsiung, Taiwan
²Providence University, Department of Food and Nutrition, Taichung, Taiwan
³Kaohsiung Medical University, Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung, Taiwan
⁴Kaohsiung Medical University, School of Pharmacy, Kaohsiung, Taiwan

Introduction:

Colorectal cancer is one of the leading causes of cancer-related deaths worldwide, highlighting the urgent need for natural compounds capable of inhibiting tumor growth and inducing cancer cell death. Sesamin, a bioactive compound derived from sesame (Sesamum indicum), is known for its health benefits, including melanin synthesis inhibition and lipid metabolism regulation.

Material and method:

This study investigates the potential anti-cancer effects and molecular mechanisms of sesamin in HCT-116 colorectal cancer cells. HCT-116 cells were treated with 0.5, 1, 2, and 3.5 mM sesamin for 48 hours to evaluate changes in cell viability, cell cycle progression, apoptosis, and the expression of related regulatory molecules.

Result and discussion:

The results showed that sesamin at concentrations above 0.5 mM significantly reduced cell viability. Treatment with >1 mM sesamin led to a significant increase in the proportion of cells in the Sub-G1 and G0/G1 phases while decreasing those in the S and G2/M phases. Sesamin at concentrations above 0.5 mM significantly increased reactive oxygen species (ROS) levels, while >1 mM sesamin significantly reduced mitochondrial membrane potential in HCT-116 cells. Additionally, sesamin at 2 and 3.5 mM significantly upregulated the mRNA expression of Bcl-2-associated X (Bax), caspase-3, -8, and -9, and enhanced apoptosis. However, there was no significant difference in the mRNA expression of B-cell lymphoma-2 (Bcl-2) and poly (ADP-ribose) polymerase (PARP) between treatment groups.

Conclusion:

In conclusion, sesamin, particularly at 2 and 3.5 mM, effectively inhibited HCT-116 cell growth by promoting apoptosis. These findings suggest that sesamin may serve as a promising bioactive compound for colorectal cancer therapy.