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Cudraxanthone D Regulates Epithelial-Mesenchymal Transition by Autophagy Inhibition in Oral Squamous Cell Carcinoma Cell Lines.
Yu, Su-Bin; Kang, Hae-Mi; Park, Dan-Bi; Park, Bong-Soo; Kim, In-Ryoung.
Afiliação
  • Yu SB; Department of Oral Anatomy, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea.
  • Kang HM; Department of Oral Anatomy, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea.
  • Park DB; BK21 PLUS Project, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea.
  • Park BS; Department of Oral Anatomy, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea.
  • Kim IR; BK21 PLUS Project, School of Dentistry, Pusan National University, 49 Busandaehak-ro, Mulguem-eup, Yangsan-si, Gyeongsangnam-do 50612, Republic of Korea.
Article em En | MEDLINE | ID: mdl-31781271
ABSTRACT
Cudraxanthone D (CD), derived from the root bark of Cudrania tricuspidata, is a natural xanthone compound. However, the biological activity of CD in terms of human metabolism has been barely reported to date. Autophagy is known as a self-degradation process related to cancer cell viability and metastasis. Herein, we investigated the effects of CD on human oral squamous cell carcinoma (OSCC) metastatic related cell phenotype. We confirmed that CD effectively decreased proliferation and viability in a time- and dose-dependent manner in human OSCC cells. In addition, OSCC cell migration, invasion, and EMT were inhibited by CD. To further determine the underlying mechanism of CD's inhibition of cell metastatic potential, we established the relationship between EMT and autophagy in OSCC cells. Thus, our findings indicated that CD inhibited the potential metastatic abilities of OSCC cells by attenuating autophagy.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2019 Tipo de documento: Article