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Mar. Drugs 2017, 15(6), 154; doi:10.3390/md15060154

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

1
Department of Biochemistry, Dong-Eui University College of Korean Medicine, Busan 47227, Korea
2
Department of Pathology, Dong-Eui University College of Korean Medicine, Busan 47227, Korea
3
Anti-Aging Research Center and Blue-Bio Industry RIC, Dongeui University, Busan 47227, Korea
4
Department of Chemistry, College of Natural Sciences, Pusan National University, Busan 46241, Korea
5
Department of Applied Research, National Marine Biodiversity Institute of Korea, Seocheon 33662, Korea
6
Department of Aquatic Life Medicine, Pukyong National University, Busan, 48513, Korea
7
Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 63243, Korea
8
Department of Microbiology, College of Medicine, Inje University, Busan 47392, Korea
9
Department of Biological Sciences, College of Natural Sciences, Pusan National University, Busan 46241, Korea
10
Departments of Parasitology and Genetics, Kosin University College of Medicine, Busan 49267, Korea
Both authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Maria Michela Corsaro
Received: 12 April 2017 / Revised: 16 May 2017 / Accepted: 22 May 2017 / Published: 30 May 2017
(This article belongs to the Special Issue Marine Oligosaccharides and Polysaccharides)
View Full-Text   |   Download PDF [2513 KB, uploaded 30 May 2017]   |  

Abstract

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. View Full-Text
Keywords: fucoidan; colorectal carcinoma; p53; G1 arrest; apoptosis fucoidan; colorectal carcinoma; p53; G1 arrest; apoptosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Park, H.Y.; Park, S.-H.; Jeong, J.-W.; Yoon, D.; Han, M.H.; Lee, D.-S.; Choi, G.; Yim, M.-J.; Lee, J.M.; Kim, D.-H.; Kim, G.-Y.; Choi, I.-W.; Kim, S.; Kim, H.-S.; Cha, H.-J.; Choi, Y.H. Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells. Mar. Drugs 2017, 15, 154.

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