Please use this identifier to cite or link to this item:
|Title:||Silencing the Metallothionein-2A gene inhibits cell cycle progression from G1- to S-phase involving ATM and cdc25A signaling in breast cancer cells||Authors:||Lim, D.
|Issue Date:||2009||Citation:||Lim, D., Jocelyn, K.M.-X., Yip, G.W.-C., Bay, B.-H. (2009). Silencing the Metallothionein-2A gene inhibits cell cycle progression from G1- to S-phase involving ATM and cdc25A signaling in breast cancer cells. Cancer Letters 276 (1) : 109-117. ScholarBank@NUS Repository. https://doi.org/10.1016/j.canlet.2008.10.038||Abstract:||Metallothioneins (MTs) are a group of metal-binding proteins involved in cell proliferation, differentiation and apoptosis. The MT-2A isoform is generally the most abundant isoform among the 10 known functional MT genes. In the present study, we observed that down-regulation of the MT-2A gene in MCF-7 cells via siRNA-mediated silencing inhibited cell growth by inducing cell cycle arrest in G1-phase (G1-arrest) and a marginal increase in cells in sub-G1-phase. Scanning electron microscopic examination of the cells with silenced expression of MT-2A (siMT-2A cells) revealed essentially normal cell morphology with presence of scattered apoptotic cells. To elucidate the underlying molecular mechanism, we examined the expression of cell cycle related genes in MT-2A-silenced cells and found a higher expression of the ataxia telangiectasia mutated (ATM) gene concomitant with a lower expression of the cdc25A gene. These data suggest that MT-2A could plausibly modulate cell cycle progression from G1- to S-phase via the ATM/Chk2/cdc25A pathway. © 2008 Elsevier Ireland Ltd. All rights reserved.||Source Title:||Cancer Letters||URI:||http://scholarbank.nus.edu.sg/handle/10635/23911||ISSN:||03043835||DOI:||10.1016/j.canlet.2008.10.038|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Sep 19, 2020
WEB OF SCIENCETM
checked on Sep 11, 2020
checked on Sep 22, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.