Article Publish Status: FREE
Abstract Title:

Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells.

Abstract Source:

Mar Drugs. 2017 May 30 ;15(6). Epub 2017 May 30. PMID: 28555064

Abstract Author(s):

Hye Young Park, Shin-Hyung Park, Jin-Woo Jeong, Dahye Yoon, Min Ho Han, Dae-Sung Lee, Grace Choi, Mi-Jin Yim, Jeong Min Lee, Do-Hyung Kim, Gi-Young Kim, Il-Whan Choi, Suhkmann Kim, Heui-Soo Kim, Hee-Jae Cha, Yung Hyun Choi

Article Affiliation:

Hye Young Park


It is well known that fucoidan, a natural sulfated polysaccharide present in various brown algae, mediates anticancer effects through the induction of cell cycle arrest and apoptosis. Nevertheless, the role of tumor suppressor p53 in the mechanism action of fucoidan remains unclear. Here, we investigated the anticancer effect of fucoidan on two p53 isogenic HCT116 (p53+/+ and p53-/-) cell lines. Our results showed that inhibition of cell viability, induction of apoptosis and DNA damage by treatment with fucoidan were similar in two cell lines. Flow cytometric analysis revealed that fucoidan resulted in G1 arrest in the cell cycle progression, which correlated with the inhibition of phosphorylation of retinoblastoma protein (pRB) and concomitant association of pRB with the transcription factor E2Fs. Furthermore, treatment with fucoidan obviously upregulated the expression of cyclin-dependent kinase (CDK) inhibitors, such as p21WAF1/CIP1 and p27KIP1, which was paralleled by an enhanced binding with CDK2 and CDK4. These events also commonly occurred in both cell lines, suggesting that fucoidan triggered G1 arrest and apoptosis in HCT116 cells by a p53-independent mechanism. Thus, given that most tumors exhibit functional p53 inactivation, fucoidan could be a possible therapeutic option for cancer treatment regardless of the p53 status.

Study Type : In Vitro Study

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