Fucoidan suppresses proliferation and epithelial‐mesenchymal transition process via Wnt/β‐catenin signalling in hemangioma

Author:

Zhu Zhengyumeng12,Luo Jialiang13,Li Lei12,Wang Di4,Xu Qishan15,Teng Jianan3,Zhou Jia2,Sun Ledong3,Yu Nansheng6,Zuo Daming1ORCID

Affiliation:

1. School of Laboratory Medicine and Biotechnology, Institute of Immunology Southern Medical University Guangzhou Guangdong China

2. Department of Immunology, School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China

3. Department of Dermatology, Guangdong Medical Products Administration Key Laboratory for Research and Evaluation of Drugs for Inflammatory Diseases, The Fifth Affiliated Hospital Southern Medical University Guangzhou Guangdong China

4. Department of Dermatology, Dermatology Hospital of Southern Medical University Southern Medical University Guangzhou Guangdong China

5. Department of Precision Laboratory Affiliated Hospital of Guangdong Medical University Zhanjiang Guangdong China

6. Department of Dermatology Affiliated Shunde Hospital of Guangzhou Medical University Foshan Guangdong China

Abstract

AbstractHemangioma is a common benign tumour that usually occurs on the skin of the head and neck, particularly among infants. The current clinical treatment against hemangioma is surgery excision, however, application of drug is a safer and more economical therapy for children suffering from hemangioma. As a natural sulfated polysaccharide rich in brown algae, fucoidan is widely recognized for anti‐tumour bioactivity and dosage safety in humans. This study aims to demonstrate the anti‐tumour effect and underlying mechanism of fucoidan against hemangioma in vivo and in vitro. We investigated the effects of fucoidan by culturing hemangioma cells in vitro and treating BALB/c mice bearing with hemangioma. At first, we measured the cell proliferation and migration ability through in vitro experiments. Then, we tested the expression of epithelial‐mesenchymal transition (EMT) and Wnt/β‐catenin pathway‐related biomarkers by western blot and qPCR. Furthermore, we applied β‐catenin‐specific inhibitor, XAV939, to determine whether fucoidan suppressed EMT via the Wnt/β‐catenin pathway in hemangioma cells. In vivo experiments, we applied oral gavage of fucoidan to treat EOMA‐bearing mice, along with evaluating the safety and efficacy of fucoidan. We found that fucoidan remarkably inhibits the proliferation and EMT ability of hemangioma cells, which is dependent on the Wnt/β‐catenin pathway. These results suggest that fucoidan exhibits tumour inhibitory effect on aggressive hemangioma via regulating the Wnt/β‐catenin signalling pathway both in vitro and in vivo, providing a new potent drug candidate for treating hemangioma.

Publisher

Wiley

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