Ethanolic extract of Halymenia durvillei induced G2/M arrest and altered the levels of cell cycle regulatory proteins of MDA-MB-231 triple-negative breast cancer cells
Issued Date
2023-05-01
Resource Type
ISSN
17355362
eISSN
17359414
Scopus ID
2-s2.0-85151642926
Journal Title
Research in Pharmaceutical Sciences
Volume
18
Issue
3
Start Page
279
End Page
291
Rights Holder(s)
SCOPUS
Bibliographic Citation
Research in Pharmaceutical Sciences Vol.18 No.3 (2023) , 279-291
Suggested Citation
Settacomkul R., Sangpairoj K., Phuagkhaopong S., Meemon K., Niamnont N., Sobhon P., Vivithanaporn P. Ethanolic extract of Halymenia durvillei induced G2/M arrest and altered the levels of cell cycle regulatory proteins of MDA-MB-231 triple-negative breast cancer cells. Research in Pharmaceutical Sciences Vol.18 No.3 (2023) , 279-291. 291. doi:10.4103/1735-5362.371584 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/81572
Title
Ethanolic extract of Halymenia durvillei induced G2/M arrest and altered the levels of cell cycle regulatory proteins of MDA-MB-231 triple-negative breast cancer cells
Other Contributor(s)
Abstract
Background and purpose: The GC-MS analysis reported n-hexadecanoic acid or palmitic acid as a major component of the ethanolic extract of Halymenia durvillei (HDET). This compound shows cytotoxic effects against various human cancer cells. The present study investigated the effect of HDET on the viability and proliferation of MDA-MB-231, a triple-negative breast cancer (TNBC) cell line. Experimental approach: Cell proliferation and cell cycle analysis were determined by flow cytometry and cell cycle regulatory protein expression levels were then determined by Western blotting. The presence of reactive oxygen species (ROS) was evaluated by dichlorofluorescein, followed by analyzing changes in gene expression of antioxidant enzymes using a real-time polymerase chain reaction. Findings/Results: HDET dose-dependently reduced cell viability with the 50% inhibitory concentration (IC 50) of 269.4 ± 31.2 μg/mL at 24 h. The cell proliferation assays showed increased succinimidyl ester fluorescent intensity after treatment with ≥ 100 μg/mL of HDET, indicating the inhibition of cell proliferation. Cell cycle analysis using propidium iodide staining showed an increased percentage of cells in the G2/M phase. HDET also decreased the levels of cell cycle regulatory proteins including cyclin D1 and increased the level of p21. HDET promoted oxidative stress by increasing ROS levels along with the reduction of catalase expression. However, HDET did not induce apoptosis and caspase activation in TNBC cells. Conclusion and implications: These findings suggest that HDET which is rich in palmitic acid may serve as a potential therapeutic agent to target TNBC via arrest cell cycle progression at the G2/M phase.