Nerolidol, Bioactive Compound Suppress Growth of HCT-116 Colorectal Cancer Cells Through Cell Cycle Arrest and Induction of Apoptosis

• Published in: Applied biochemistry and biotechnology 2024-03, Vol.196 (3), p.1365-1375
• Main Authors: Zhao, Xiaoqian, Chinnathambi, Arunachalam, Alharbi, Sulaiman Ali, Natarajan, Nandakumar, Raman, Muthusamy
• Format: Article
• Language: English
• Subjects: 4',6-diamidino-2-phenylindole; Accumulation; Apoptosis; Assaying; Bioactive compounds; Biochemistry; Biocompatibility; Biotechnology; Cell Cycle; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Cell viability; Chemistry; Chemistry and Materials Science; Colon; Colon cancer; Colonic Neoplasms; Colorectal cancer; Colorectal carcinoma; colorectal neoplasms; Cytotoxicity; Female; Flow cytometry; G1 phase; HCT116 Cells; health services; Humans; inhibitory concentration 50; mortality; Nerolidol; Original Article; Reactive Oxygen Species - metabolism; Sesquiterpenes; Staining
• ISSN: 0273-2289; 1559-0291
• DOI: 10.1007/s12010-023-04612-9

Colon cancer is the most prevalent cancer and causes the highest cancer-associated mortality in both men and women globally. It has a high incidence and fatality rate, which places a significant burden on the healthcare system. The current work was performed to understand the beneficial roles of nerolidol on the viability and cytotoxic mechanisms in the colon cancer HCT-116 cells. The MTT cytotoxicity assay was done to investigate the effect of nerolidol at different doses (5–100 µM) on the HCT-116 cell viability. The impacts of nerolidol on ROS accumulation and apoptosis were investigated using DCFH-DA, DAPI, and dual staining assays, respectively. The flow cytometry analysis was performed to study the influence of nerolidol on the cell cycle arrest in the HCT-116 cells. The outcomes of the MTT assay demonstrated that nerolidol at different doses (5–100 µM) substantially inhibited the HCT-116 cell viability with an IC50 level of 25 µM. The treatment with nerolidol appreciably boosted the ROS level in the HCT-116 cells. The findings of DAPI and dual staining revealed higher apoptotic incidences in the nerolidol-exposed HCT-116 cells, which supports its ability to stimulate apoptosis. The flow cytometry analysis demonstrated the considerable inhibition in cell cycle at the G0/G1 phase in the nerolidol-exposed HCT-116 cells. Our research showed that nerolidol can inhibit the cell cycle, increase ROS accumulation, and activate apoptosis in HCT-116 cells. In light of this, it may prove to be a potent and salutary candidate to treat colon cancer.