J Med Life Sci > Volume 17(2); 2020 > Article
Journal of Medicine and Life Science 2020;17(2):41-46.
DOI: https://doi.org/10.22730/jmls.2020.17.2.41    Published online August 31, 2020.
Metformin에 의해 발생한 H4IIE 간암세포의 세포사멸 과정에서 자가포식의 역할
백근호, 박덕배
제주대학교 의학전문대학원 의학과
Role of autophagy in metformin-induced apoptosis of H4IIE hepatocellular carcinoma cells
Keunho Baek, Deokbae Park
Department of Medicine, School of Medicine, Jeju National University, 102 Jejudaehakro, Jeju 63243, Republic of Korea
Correspondence:  Deokbae Park, Tel: 82-64-753-3827,  Email: parkdb@jejunu.ac.kr
Metformin, a predominantly prescribed anti-diabetic drug for decades, has gained new insights for its anti-tumor activity in a variety of cancer cells. Our previous studies also showed the obvious pro-apoptotic activity of metformin and the underlying action mechanisms in hepatocellular carcinoma cells. Together with apoptosis, autophagy is a crucial intracellular process to determine the survival or death of cells under some stressful environments. The present study aimed to determine the role of autophagy in metformin-induced death of H4IIE hepatocellular carcinoma cells. Metformin blocked the formation of autophagosomes and the expression of LC3A, generally described as biomarkers of autophagy. Inhibition of AMPK reversed the metformin-induced blockade of autophagy. Antioxidant (NAC) suppressed the metformin-induced cell death but not affected LC3A. The inhibition of protein kinase C totally restored the metformin-suppressed expression of LC3A. In summary, our present study suggests that autophagy is an anti-apoptotic player in metformin-induced apoptosis if H4IIE cells.
Key Words: Metformin, Apoptosis, Autophagy, H4IIE
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