Anti-leukemic effect of a synthetic compound, (+/-) trans-dihydronarciclasine (HYU-01) via cell-cycle arrest and apoptosis in acute myeloid leukemia
- Authors
- Kim, Seo Ju; Park, Hyun Ki; Kim, Ju Young; Yoon, Jin Sun; Kim, Eun Shil; Cho, Cheon-Gyu; Kim, Byoung Kook; Park, Byeong Bae; Lee, Young Yiul
- Issue Date
- Oct-2012
- Publisher
- WILEY-BLACKWELL
- Keywords
- HYU-01; (+/-) trans-dihydronarciclasine; cell cycle; apoptosis; p27; acute myeloid leukemia
- Citation
- APMIS, v.120, no.10, pp.836 - 845
- Indexed
- SCIE
SCOPUS
- Journal Title
- APMIS
- Volume
- 120
- Number
- 10
- Start Page
- 836
- End Page
- 845
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/164551
- DOI
- 10.1111/j.1600-0463.2012.02916.x
- ISSN
- 0903-4641
- Abstract
- (+/-) trans-Dihydronarciclasine, isolated from Chinese medicinal plant Zephyranthes candida, has been shown to possess quite potent anti-tumoral effect against selected human cancer cell lines. However, little is known about the anti-tumoral effect of (+/-) trans-dihydronarciclasine in acute myeloid leukemia (AML). This study was performed to investigate the effect of a novel synthetic (+/-) trans-dihydronarciclasine (code name; HYU-01) in AML. The HYU-01 inhibited the proliferation of various AML cell lines including HL-60 as well as primary leukemic blasts in a dose-dependent manner. To investigate the mechanism of the anti-proliferative effect of HYU-01, cell-cycle analysis was attempted in HL-60 cells, resulting in G1 arrest. The expression levels of CDK2, CDK4, CDK6, cyclin E, and cyclin A were decreased in a time-dependent manner. In addition, HYU-01 up-regulated the expression of the p27, and markedly enhanced the binding of p27 with CDK2, 4, and 6, ultimately resulting in the decrease of their kinase activities. Furthermore, HYU-01 induced the apoptosis through the induction of proapoptotic molecules and reduction of antiapoptotic molecules in association with the activation of caspase-3, -8, and -9. These results suggest that HYU-01 may inhibit the proliferation of HL-60 cells, via apoptosis, as well as G1 block in association with the induction of p27.
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