Page 114 - ebook

[A. Biochemistry/Molecular Biology] A-57

Mechanism Of Juglone-induced Apoptosis In p53 Null Non-

Small Cell Lung Cancer

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Won Ho Kim¹ , So-Jung Kim² , Minseok Kwak³*, Jun-O Jin²*, Peter Chang-Whan Lee¹*
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¹Biomedical Sciences, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea, ²Medical

Biotechnology, Yeungnam University, Gyeongsan 38541, Korea, ³Chemistry, Pukyong National University, Busan

48513, Korea

Lung cancer is one of the most common cancers, and non-small cell lung cancer (NSCLC) accounts for more than
80% of them. TP53 is the most common mutated gene associated with human cancer and p53-mutated cancer

cells frequently grow more aggressively than those with wild-type p53. A line of evidence has been shown that
Juglone (5-hydroxy-1,4-naphthalenedione), an organic compound, exhibits cytotoxicity against some cancer cells.

However, its mechanism has not been investigated well. This study aimed to explore the mechanism of Juglone-
induced apoptosis in lung cancer cells. Here, we found that Juglone significantly inhibited cell viability in p53-null

H1299 cells, whereas no effect was observed in A549 cells with wild-type p53. In addition, it was confirmed that
DNA fragmentation occurs through Juglone. Migration ability was also significantly inhibited in H1299 cells after

Juglone treatment. We further observed that Juglone cytotoxicity in H1299 cells upregulation of cleaved-PARP,
cleaved-Caspase-3, But A549 cells were not cytotoxicity. Our results illustrated that Juglone caused apoptosis in

lung cancer cells and this effect is independent of p53. Thus, our study suggested that Juglone might be considered
as an effective strategy for TP53 mutation lung cancer therapy.