Impact of let-7g on Proliferation and Lactation of Mouse Mammary Epithelial Cells

let-7g, a member of the let-7 family, regulates gene expression at the post-transcriptional level. The study explored a series of biological effects of mouse mammary epithelial cells that let-7g was produced. The differential expression of let-7g was detected by qRT-PCR in different developmental stages of the mouse mammary gland, let-7g expression and impact of let-7g on mouse mammary epithelial cells were analyzed by CASY-technology, qRT-PCR, Western blotting and HPLC inhibited let-7g expression of mouse mammary epithelial ceils through gene silencing. The results showed that qRT-PCR identified let-7g as being down-regulated in mouse mammary epithelial cells after it was inhibited. Mouse mammary epithelial cells with low expression of let-7g displayed higher expression of TGFβR I protein than those with high expression of let-7g, suggesting that low let-7g expression contributed to TGFβR I over-expression. Finally, the expression of let-7g was down-regulated, which significantly enhanced the proliferation of mouse mammary epithelial cells, and increased expression of β-Casein. The data indicated that let-7g could negatively regulate the expression of target Tgfbrl by complementary combination in mouse mammary epithelial cells, and then regulate the cell proliferation and expression of β-Casein by suppressing the TGFβR I expression.

The effects of thyroid-stimulating hormone,estradiol and prolactin on sodium/iodide symporter mRNA expression in mouse lactating mammary gland cells under different iodine levels

Objective The present study investigated the sodium/iodide symporter mRNA expression in mouse lactating mammary gland cells under different iodine levels and the effects of thyroid-stimulating hormone(TSH),estradiol(E2)and prolactin(PRL)on NIS mRNA expression in mouse lactating mammary gland cells.

Ganoderma lucidum polysaccharide inhibits LPS-induced inflammatory injury to mammary epithelial cells

This study sought to investigate whether Ganoderma lucidum polysaccharide(GLP)has a protective effect on lipopolysaccharide(LPS)-induced inflammatory injury to mammary epithelial HC-11 cells and to characterize the mechanism involved.Cell viability was assessed using the cell counting kit 8(CCK-8)method,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and IL-1βlevels were measured by enzyme linked immunosorbent assay(ELISA),and IκBa,p65 NF-κB and STAT3 mRNA were determined using quantitative reverse transcription PCR(qRT-PCR),p65 and STAT3 protein expression were determined using Western blotting,respectively.GLP was shown to inhibit LPS-induced TNF-α,IL-6,and IL-1βproduction(P<0.01 or P<0.05),GLP was also shown to increase IκBαmRNA expression(P<0.01),decrease p65 and STAT3 mRNA expression(P<0.01 or P<0.05),and decrease p-p65,p65,p-STAT3,and STAT3 protein expression in breast epithelial cells(P<0.01 or P<0.05).The findings suggest that GLP inhibits nuclear factor kappa-B(NF-κB)and signal transducers and activators of transcription(STAT)signaling by preventing IκBαdegradation and p65 and STAT3 phosphorylation.This results in lower LPS-induced TNF-α,IL-6,and IL-1βproduction and prevents inflammatory cell injury.