Dieckol induces cell cycle arrest by down‐regulating CDK2/cyclin E in response to p21/p53 activation in human tracheal fibroblasts. (27th October 2021)

• Record Type: Journal Article
• Authors: Heo, Seong‐Yeong; Jeong, Min‐Seon; Lee, Hyoung Shin; Park, Won Sun; Choi, Il‐Whan; Yi, Myunggi; Jung, Won‐Kyo
• Is Part Of: Cell biochemistry and function. Volume 40:Number 1(2022)
• Page Start: 71
• Page End: 78
• Publication Date: 2021-10-27
• Subjects: cell cycle arrest -- cyclin E/CDK2 complex -- Dieckol -- Ecklonia cava -- human tracheal fibroblasts; Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3675
• Languages: English
• ISSNs: 0263-6484

Abstract

Abstract : The phlorotannin derivative dieckol isolated from Ecklonia cava has been shown to exhibit anti‐inflammatory, anti‐bacterial, anti‐oxidative anti‐adipogenic and anti‐stenosis activity. However, the role of dieckol in cyclin‐dependent kinase 2 (CDK2)/cyclin E signalling, which regulates fibrosis development, has not yet been determined. In this study, we report that dieckol‐suppressed cell proliferation through the cell cycle arrest of Hs680.Tr human tracheal fibroblasts. Following consecutive purification, dieckol was identified as a potent bioactive compound. The results showed that dieckol had significant anti‐proliferative activity against Hs680.Tr human tracheal fibroblastsWestern blotting analysis also found that dieckol dose‐dependently induced the cell cycle arrest of Hs680.Tr fibroblasts in the G0/G1 phase, accompanied by the downregulation of CDK2 and cyclin E and the upregulation of p21 and p53. As attested by molecular docking study, the dieckol interacted with the core interface residues in transforming growth factor‐β receptor with high affinity. These findings suggest that dieckol from E. cava inhibits the cell proliferation of Hs680.Tr, potentially through p21‐ and p53‐mediated G0/G1 cell cycle arrest.