Prolactin regulation of beta-casein gene expression and of a cytosolic 120-kd protein in a cloned mouse mammary epithelial cell line.

Ball, Roland K.; Friis, Robert R.; Schoenenberger, Cora‐Ann; Doppler, Wolfgang; Groner, Bernd

doi:10.1002/j.1460-2075.1988.tb03048.x

Cited by 468 publications

(370 citation statements)

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“…Due to the lack of a suitable cell system for mechanistic study, most of the regulatory studies on LF were conducted in animals and in transiently transfected culture cell lines [7,17,37,38]. HC-11 is a normal mouse mammary gland cell line which retains the normal phenotype of mammary gland epithelial cells [29]. In addition, the LF gene is functional and can be regulated by hormones and an innate immune stimuli in this cell type (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The HC-11 mouse mammary gland cell line, originally cloned from the COMMA-D1 cell line from a mid-pregnant BALB/c mouse [29], retains many of the normal features of mammary gland epithelial cells [30] including intact Toll-like receptor-mediated signaling pathway [7]. Lactoferrin is expressed in the HC-11 cells and responded to estrogen stimulation (Fig.…”

Section: Lps and Dsrna Induces Lf Expressions In The Hc-11 Mammary Epmentioning

confidence: 99%

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Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Limmon

Imani

et al. 2009

Biochimie

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Lactoferrin (LF) is a multifunctional protein. While its functions and mechanism of actions are actively being investigated, the cellular signals that regulate LF expression have not been as explored. We have previously demonstrated that LF is upregulated by estrogen in reproductive system. In this study, we show that the expression of LF was stimulated by bacterial lipopolysaccharide (LPS) and double-stranded RNA (dsRNA) in normal mouse mammalian HC-11 cells. When cells were exposed to either LPS or dsRNA, the mRNA and protein of LF were increased in a dose-and time-dependent manner, yet the kinetics of LF induction by dsRNA or LPS was different. The LPS and dsRNAinduced LF was mainly released into the culture medium where it blocked TNF-α production in exposed cells. We explored the mechanisms of LF induction by LPS and dsRNA using specific inhibitors and found that the induction could be attenuated by inhibitors to PKC, NF-kB, p38 and JNK, but not by an inhibitor to PKA. Interestingly, ERK inhibitor was effective against dsRNA but not against LPS induction of LF. These data suggest that LF was induced by LPS and dsRNA through PKC, NF-kB and MAPK pathways which in turn plays an inhibitory role in the continuation of innate inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Lps and Dsrna Induces Lf Expressions In The Hc-11 Mammary Epmentioning

confidence: 99%

Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Limmon

Imani

et al. 2009

Biochimie

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“…The expression of Runx2 in HC11 cells is particularly interesting because these cells do not originate from a tumor but are derived from the mammary gland of a pregnant mouse [Ball et al, 1988]. In contrast to the cancer cell lines they retain the ability to produce milk proteins in response to lactogenic hormones and have been used extensively as a model to investigate mammary gland-specific gene regulation.…”

Section: A Role For Runx2 In Normal Mammary Glandmentioning

confidence: 99%

A role for Runx2 in normal mammary gland and breast cancer bone metastasis

Shore

2005

J of Cellular Biochemistry

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The transcription factor Runx2 is essential for the formation of the skeleton. It has therefore primarily been considered as a specific regulator of bone genes. However, mice containing a LacZ insertion at the Runx2 locus also revealed expression in the nascent mammary epithelium. Reports of Runx2 expression in breast cancer cell lines, combined with the fact that breast cancers preferentially metastasise to bone, have also hinted at a potential role for Runx2 in the formation of bone metastasese. These initial observations have prompted further analysis of Runx2 function in mammary epithelial cells and recent findings have demonstrated that Runx2 does indeed contribute to the ability of metastatic breast cancer cell lines to form osteolytic bone lesions. In addition, evidence is accumulating that Runx2 has a role in the regulation of normal mammary gland gene expression and recent data demonstrate that it regulates transcription of the mammary gland-specific gene, b-casein. In this article I discuss recent advances that link Runx2 with normal mammary epithelial cell function and the development of bone metastasese in breast cancer.

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“…HC11 mouse mammary epithelial cells (Ball et al, 1988) were grown in RPMI-1640 (Gibco ± BRL) containing 10% FCS (HyClone Laboratories, Inc.), 5 mg/ml insulin and 10 ng/ml murine natural EGF (Sigma). The packaging cell line Bosc 23 (Pear et al, 1993) was maintained in DMEM (Gibco ± BRL) containing 10% FCS.…”

Section: Cellsmentioning

confidence: 99%