Ethyl Acetate Extract of Halymenia durvillei Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells
Issued Date
2023-03-01
Resource Type
ISSN
22871098
eISSN
22878602
Scopus ID
2-s2.0-85159348202
Journal Title
Preventive Nutrition and Food Science
Volume
28
Issue
1
Start Page
69
End Page
78
Rights Holder(s)
SCOPUS
Bibliographic Citation
Preventive Nutrition and Food Science Vol.28 No.1 (2023) , 69-78
Suggested Citation
Chantree P., Martviset P., Sornchuer P., Thongsepee N., Sangpairoj K., Meemon K., Niamnont N., Tamtin M., Sobhon P. Ethyl Acetate Extract of Halymenia durvillei Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells. Preventive Nutrition and Food Science Vol.28 No.1 (2023) , 69-78. 78. doi:10.3746/pnf.2023.28.1.69 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/82818
Title
Ethyl Acetate Extract of Halymenia durvillei Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells
Other Contributor(s)
Abstract
Colorectal cancer is one of the most death-dealing cancers. However, conventional cancer treatments still have side effects. Therefore, novel chemotherapeutic agents with less side effects are still in search. A marine red seaweed, Halymenia durvillei, is recently interested in its anticancer effects. This study investigated the anticancer effect of ethyl acetate extract of H. durvillei (HDEA) on HT-29 colorectal cancer cells in association with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. HDEA-treated HT-29 and OUMS-36 cells were used for cell viability tests by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide assay. The effects of HDEA on apoptosis and cell cycle were evaluated. The nuclear morphology and mitochondrial membrane potential (∆ψm) were observed by Hoechst 33342 and JC-1 staining, respectively. The gene expression of PI3K, AKT, and mTOR genes was evaluated using a real-time semiquantitative reverse transcription-polymerase chain reaction. The corresponding protein expressions were assessed by western blot analysis. The result revealed that the cell viability of treated HT-29 cells diminished while that of OUMS-36 cells was non-significant. By the down-regulation of cyclin-dependent kinase 4 and cyclin D1, HDEA-treated HT-29 cells were arrested in the G0/G1 phase. By the up-regulation of cleaved poly(adenosine diphosphate-ribose) polymerase, caspase-9, caspase-8, caspase-3, and Bax, HDEA-treated HT-29 cells underwent apoptosis, but suppressed Bcl-2, disrupted nuclear morphology and ∆ψm. Furthermore, treated HT-29 cells underwent autophagy by up-regulation of light chain 3-II and beclin-1. Lastly, HDEA suppressed the expression of PI3K, AKT, and mTOR. Therefore, HDEA exerts anticancer effects against HT-29 cells, confirmed by apoptosis, autophagy, and cell cycle arrest induction via regulation of the PI3K/AKT/mTOR signaling pathway.