Growth Factor Regulation of Cell Cycle Progression in Mammary Epithelial Cells

Stull, Malinda A.; Rowzee, Anne; Loladze, Aimee V.; Wood, Teresa L.

doi:10.1023/b:jomg.0000023585.95430.f4

Cited by 39 publications

(28 citation statements)

References 66 publications

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“…Our data clearly demonstrate that PRP induced increases in cell migration, and proliferation rates, as well as an increase in the expression of G1 cell cycle regulatory proteins, such as cyclin A, Cdk2, and cyclin E in HSF. Accumulating data indicate that growth factors and cytokines control cell proliferation through regulation of cell cycle progression (19). Growth factors promote entry into and progression through the cell cycle by regulating expression levels and activation of cyclin-Cdks.…”

Section: Discussionmentioning

confidence: 99%

Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts

Cho

Kim²,

Lee

2011

Int J Mol Med

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Abstract. Platelet-rich plasma (PRP) is derived from fresh whole blood, which contains a high concentration of platelets. Recently, PRP has been used for skin wound healing and rejuvenation. However, the molecular mechanisms underlying PRP-inducing wound healing processes are still largely unknown. The aim of this study is to evaluate the effect of PRP on the expression of G1 cell cycle regulatory proteins, type I collagen, matrix metalloproteinase-1 (MMP-1), and MMP-2 in human skin fibroblasts (HSF). We performed a cell proliferation and a migration assay, immunoblotting, and a chloramphenicol acetyltransferase (CAT) assay in PRP-treated human skin fibroblasts. PRP treatment induced increased rates of cell proliferation and cell migration. Expression of cyclin A protein was increased by a low concentration (0.5%) of PRP-treated HSF. In addition, expression of Rb, cyclin E, and cyclin-dependent kinase 4 proteins was increased by a high concentration (5%) of PRP-treated HSF. High concentration of PRP induced an up-regulation of type I collagen, MMP-1, and MMP-2 expression in HSF. Taken together, PRP treatment induced an increase in expression of G1 cell cycle regulators, type I collagen and MMP-1, thereby accelerating the wound healing process.

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Section: Discussionmentioning

confidence: 99%

Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts

Cho

Kim²,

Lee

2011

Int J Mol Med

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“…Cyclin A is upregulated in S and G 2 phase and downregulated in G 1 . Cyclin D expression is induced during early G 1 as cells exit G 0 , when it forms a complex with cdk4/6 and phosphorylates pRb, and is thus critical for cell cycle activation (Stull et al, 2004). Levels of cyclin D remain high throughout the remainder of the cell cycle.…”

Section: 1b Inhibits Mammary Epithelial Cell Proliferation But Doesmentioning

confidence: 99%

Protein 4.1B expression is induced in mammary epithelial cells during pregnancy and regulates their proliferation

et al. 2005

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4.1B is a member of the protein 4.1 superfamily of proteins that link transmembrane proteins to the actin cytoskeleton. The 4.1B gene localizes to chromosome 18p11.3, which undergoes loss of heterozygosity in mammary tumors. Here, we examine the expression of 4.1B in murine mammary epithelium and find that 4.1B is dramatically upregulated in mammary epithelial cells during pregnancy when there is extensive cell proliferation. In contrast, 4.1B is not expressed in virgin, lactating, or involuting mammary epithelium. To examine the consequence of 4.1B loss on mammary epithelial cell proliferation, we analysed mammary glands in 4.1B-null mice. 4.1B loss results in a significant increase in mammary epithelial cell proliferation during pregnancy, but has no effect on mammary epithelial cell proliferation, in virgin or involuting mice. Furthermore, we show that 4.1B inhibits the proliferation of mammary epithelial cell lines by inducing a G 1 cell cycle arrest, characterized by decreased cyclin A expression and reduced Rb phosphorylation, and accompanied by reduced erbB2 phosphorylation. This cell cycle arrest does not involve alterations in the activities of MAPK, JNK, or Akt. Collectively, our findings demonstrate that 4.1B regulates mammary epithelial cell proliferation during pregnancy and suggest that its loss may influence mammary carcinoma pathogenesis in multiparous women.

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“…The INK4 family members (p15 Ink4B , p16 Ink4A , p18 Ink4C and p19 Ink4D ) specifically bind and inhibit CDK4,6 during the G 1 phase of the cell cycle, while KIP/CIP family members (p21 Cip1 , p27 Kip1 and p57 Kip2 ) can inhibit CDK activity during all phases of the cell cycle. 8 Both families of CDKIs have been shown to play regulatory roles at the G 1 /S cell cycle checkpoint.…”

Section: Introductionmentioning

confidence: 99%

Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues

Eigėlienė¹,

Härkönen²,

Erkkola³

2008

Cell Cycle

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Growth Factor Regulation of Cell Cycle Progression in Mammary Epithelial Cells

Cited by 39 publications

References 66 publications

Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts

Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts

Protein 4.1B expression is induced in mammary epithelial cells during pregnancy and regulates their proliferation

Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues

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