Upregulation of autophagy by Ginsenoside Rg2 in MCF-7 cells

• Published in: Animal cells and systems Vol. 22; no. 6; pp. 382 - 389
• Main Authors: Chung, Yuheon, Jeong, Seula, Choi, Hyun Seok, Ro, Seungil, Lee, Jung Sup, Park, Jong Kun
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 02.11.2018; Taylor & Francis Ltd; Taylor & Francis Group; 한국통합생물학회
• Subjects: Autophagy; Breast cancer; Cell survival; Cyclobutane; Cytotoxicity; Deoxyribonucleic acid; Dimers; DNA; DNA damage; DNA repair; Genotoxicity; Ginseng; Ginsenoside Rg2; Ginsenosides; MCF-7; Modulation; Molecular & Cellular Biology; p53 Protein; Phagocytosis; Proteins; Toxicity; Ultraviolet radiation; Up-regulation; UVB; 생물학; UVB; Ginsenoside Rg2; Autophagy; MCF-7
• ISSN: 1976-8354; 2151-2485
• DOI: 10.1080/19768354.2018.1545696

Autophagy is a major intracellular degradation process that plays an important role in cell survival, stress responses, nutrient sensing and development. Our previous studies have shown that Rg2, a triterpenoid saponin contained in ginseng, protects cells against UVB-induced genotoxicity by increasing DNA repair, in possible association with modulation of protein levels involved in p53 pathway. In this study, we determined an upregulation of autophagy by Rg2. Rg2 treatment for 24 h in MCF-7, a breast cancer cell, did not show cytotoxicity up to 200 μM. Rg2 also upregulated the level of p-p53, p-AMPK, p-ACC, Atg-7 and LC3-II and decreased the level of p62 in concentration-dependent manners. We also determined the level of p53, AMPK, p62, Atg-7 and LC3 after UVB exposure and subsequent incubation in growth medium for 24 h. UVB increased the level of p-p53, p-AMPK, p-ACC and decreased the levels of p62, Atg-7 and LC3-II. Interestingly, Rg2 treatment for 24 h after UVB exposure increased the levels of p-p53, p-AMPK, p-ACC, Atg-7 and LC3-II and decreased the level of cyclobutane pyrimidine dimer, a UVB-induced DNA damage in concentration-dependent manners. All these results suggest that Rg2 increased autophagy and decreased UVB-induced DNA damage, in possible association with the modulation of protein levels in p53- and autophagic pathways.