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Iron-saturated lactoferrin stimulates cell cycle progression through PI3K/Akt pathway

Authors
Lee, Shin-HeePyo, Chul-WoongHahm, Dae HyunKim, JiyoungChoi, Sang-Yun
Issue Date
7월-2009
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Keywords
Akt; cell cycle; lactoferrin; p21Cip/WAF1; p27kip1
Citation
MOLECULES AND CELLS, v.28, no.1, pp.37 - 42
Indexed
SCIE
SCOPUS
KCI
Journal Title
MOLECULES AND CELLS
Volume
28
Number
1
Start Page
37
End Page
42
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/119751
DOI
10.1007/s10059-009-0102-3
ISSN
1016-8478
Abstract
Iron binding lactoferrin (Lf) is involved in the control of cell cycle progression. However, the molecular basis underlying the effects of Lf on cell cycle control, as well as its target genes, remains incompletely understood. In this study, we have demonstrated that a relatively low level of ironsaturated Lf, Lf(Fe3+), can stimulate S phase cell cycle entry, and requires Akt activation in MCF-7 cells. Lf(Fe3+) immediately induced Akt phosphorylation at Ser473, which subsequently induced the phosphorylation of two G1-checkpoint Cdk inhibitors, p21(Cip/WAF1) and p27(kip1). The Lf(Fe3+)-induced phosphorylation of Cdk inhibitors impaired their nuclear import behavior, thereby inducing cell cycle progression. However, the treatment of cells with a PI3K inhibitor, LY294002, almost completely blocked Lf(Fe3+)-stimulated cell cycle progression. LY294002 treatment abrogated Lf(Fe3+)-induced Akt activation, and prevented the cytoplasmic localization of p27(kip1). Higher levels of p21(Cip/WAF1) were also detected in the cytoplasmic sub-cellular compartment as a measure of cellular response to Lf(Fe3+). Consequently, the degree of phosphorylation of retinoblastoma protein was enhanced in response to Lf(Fe3+). Therefore, we conclude that Lf(Fe3+), as a potential antagonist of Cdk inhibitors, can facilitate the functions of E2F during progression to S phase via the Akt signaling pathway.
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