Sulfated galactan derivatives from Gracilaria fisheri suppress the proliferation of MCF-7 breast cancer cells by inducing cell cycle arrest
1
Issued Date
2025-01-01
Resource Type
ISSN
26322900
eISSN
26322919
Scopus ID
2-s2.0-105014994913
Journal Title
World Academy of Sciences Journal
Volume
7
Issue
5
Rights Holder(s)
SCOPUS
Bibliographic Citation
World Academy of Sciences Journal Vol.7 No.5 (2025)
Suggested Citation
Phanphak J., Somintara S., Sakaew W., Senarai T., Kovensky J., Wongprasert K., Rudtanatip T. Sulfated galactan derivatives from Gracilaria fisheri suppress the proliferation of MCF-7 breast cancer cells by inducing cell cycle arrest. World Academy of Sciences Journal Vol.7 No.5 (2025). doi:10.3892/wasj.2025.365 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/112020
Title
Sulfated galactan derivatives from Gracilaria fisheri suppress the proliferation of MCF-7 breast cancer cells by inducing cell cycle arrest
Corresponding Author(s)
Other Contributor(s)
Abstract
Breast cancer is one of the most prevalent diseases affecting the female population, with its incidence increasing globally. Previous studies have identified cyclins, CDKs and upstream signaling molecules as key therapeutic targets, as their overexpression can drive the transformation of normal cells into cancerous ones. Sulfated galactan (SG), a polysaccharide derived from Gracilaria fisheri, has demonstrated potential in modulating cellular functions. Recent research suggests that low molecular weight SG (LSG), when supplemented with an octanoyl ester (LSGO), exhibits an enhanced biological activity. However, the anticancer effects of SG and its derivatives in breast cancer remain underexplored. The present study thus aimed to examine the effects of SG, LSG and LSGO on MCF-7 breast cancer cells. Cytotoxicity was initially assessed in L929 normal fibroblast cells and MCF-7 cells. While all three forms were non-toxic to L929 cells, LSGO exhibited slight cytotoxicity and significantly induced cell cycle arrest at the G2/M phase. Mechanistically, LSGO suppressed the PI3K/AKT/mTOR and ERK pathways, downregulated cyclins and CDKs, and led to cell cycle arrest and reduced cell proliferation. These results suggest that the structural modification of SG enhances its anti-proliferative capacity, highlighting LSGO as a promising candidate for the treatment of MCF-7 cells. Overall, these findings provide insight into the molecular mechanisms by which SG derivatives affect breast cancer cell proliferation and underscore their potential as anti-proliferative agents targeting cell cycle regulatory proteins.