Induction of Apoptosis and Inhibition of Epithelial Mesenchymal Transition by α-Mangostin in MG-63 Cell Lines

Author:

Park Sung-Jin1,Park Bong-Soo12ORCID,Yu Su-Bin12ORCID,Kang Hae-Mi12,Kim Hye-Jin3ORCID,Kim In-Ryoung1ORCID

Affiliation:

1. Department of Oral Anatomy, School of Dentistry, Pusan National University, Busandaehak-ro 49, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea

2. BK21 PLUS Project, School of Dentistry, Pusan National University, Busandaehak-ro 49, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea

3. Department of Dental Hygiene, Dongeui University, Gaya 1-dong, Busanjin-gu, Busan 47230, Republic of Korea

Abstract

Osteosarcoma is the most common bone primary malignant tumor and nearly 30% of patients still die from osteosarcoma due to metastasis or recurrence. Thus, it is necessary to develop effective new chemotherapeutic agents for osteosarcoma treatment. α-Mangostin is a xanthone derivative shown to have antioxidant and anticarcinogen properties. However, the molecular mechanisms underlying the antimetastatic effects of osteosarcoma remain unclear. In metastasis progression, epithelial mesenchymal transition (EMT) is a process that plays important roles in development, cell polarity, and increased invasion and migration. This study focused on the induction of apoptosis and inhibition of EMT process by α-mangostin in human osteosarcoma cell line MG63. α-Mangostin treatments on MG63 cells not only showed the several lines of evidence of apoptotic cell death but also inhibited cell migration, invasion, and EMT-inducing transcription factor. In conclusion, we demonstrate that the α-mangostin induces apoptosis via mitochondrial pathway and suppresses metastasis of osteosarcoma cells by inhibiting EMT.

Funder

National Research Foundation of Korea

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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