Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Baratta, Mario; Grolli, Stefano; Poletti, Angelo; Ramoni, Roberto; Motta, Manuela; Tamanini, Carlo

doi:10.1677/joe.0.1670053

Cited by 32 publications

(13 citation statements)

References 28 publications

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“…Mammary epithelial cell line HC11 was able to differentiate and induce expression of the β-casein gene when stimulated with lactogenic hormones for 72 h. As previously reported (Baratta et al, 2000) treatment of confluent cultures with differentiation medium containing the lactogenic hormones dexamethasone, insulin and prolactin led to a dose-dependent induction of β-casein mRNA expression, while proliferating cells or HC11 cultured in differentiation medium lacking prolactin expressed very low levels of β-casein mRNA. In confluent HC11 cells, addition of CURC (100 ng) influenced significantly the induction of β-casein mRNA levels analysed by real time PCR (Figure 8).…”

Section: Effect Of Curc On β-Casein Gene Expression In Differentiatinsupporting

confidence: 74%

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Curcuminoid-phospholipid complex induces apoptosis in mammary epithelial cells by STAT-3 signaling

et al. 2008

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Curcumin (from the rhizome of Curcuma longa) is well documented for its medicinal properties in Indian and Chinese systems of medicine where it is widely used for the treatment of several diseases. Epidemiological observations are suggestive that curcumin consumption may reduce the risk of some form of cancers and provide other protective biological effects in humans. These biological properties have been attributed to curcuminoids that have been widely studied for their anti-inflammatory, anti-angiogenic, antioxidant, wound healing and anti-cancer effects. In this study we have investigated on the effect of a curcumin phospholipid complex on mammary epithelial cell viability. HC11 and BME-UV cell lines, validated models to study biology of normal, not tumoral, mammary epithelial cells, were used to analyse these effects. We report that curcumin acts on STAT-3 signal pathway to reduce cell viability and increase apoptosis evaluated by the the amount of activated caspase 3. Further it reduces MAPK and AKT activations. JSI-124, a STAT-3 inhibitor (100 nM) was able to block the negative effect of curcumin on cell viability and caspase 3 activation. Finally the negative effect of cucumin on cell viability has been impaired in STAT-3 i HC11, where STAT-3 protein was greatly reduced by shRNA-interference. These results indicate that curcumin presents a potential adverse effect to normal mammary epithelial cells and that it has a specific effect on signal trasduction in mammary epithelium.

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Section: Effect Of Curc On β-Casein Gene Expression In Differentiatinsupporting

confidence: 74%

“…Subsequently, the cells were incubated for up to 4 days in differentiation medium [RPMI 1640 medium containing 3% FCS and the lactogenic hormones dexamethasone (1 μM), insulin (5 μg/ml) and prolactin (5 μg/ml)]. Differentiation was monitored by measuring expression of the milk protein β-casein (Baratta et al, 2000).…”

Section: Cell Culturementioning

confidence: 99%

Curcuminoid-phospholipid complex induces apoptosis in mammary epithelial cells by STAT-3 signaling

et al. 2008

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“…All of these cell lines exhibited testosterone regulation of either Clu or MMTV, except for HC11 (Fig. 1A); however, HC11 previously was shown to contain androgen receptors and to respond to androgen stimulation (Baratta et al, 2000). These results indicate that although these five cell lines did not express Fgf8 in response to testosterone, they do retain the ability to respond to exogenous androgens.…”

Section: Negative Control Gapdh Pcrs Are Shown (-Rt) (C) Rt-pcr Analmentioning

confidence: 82%

Androgen inducibility of Fgf8 in Shionogi carcinoma 115 cells correlates with an adjacent t(5;19) translocation

Erdreich‐Epstein

Ganguly

Shi

et al. 2005

Genes Chromosomes & Cancer

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Fgf8 (fibroblast growth factor 8) was initially cloned from a mouse mammary tumor cell line derived from the androgen-dependent Shionogi carcinoma 115. The androgen-inducible expression of Fgf8 in this tumor controls its androgen-dependent phenotype, thus stimulating interest in this gene as a possible factor in human prostate cancer and other androgen-sensitive cancers. However, apart from Shionogi carcinoma 115, the androgen inducibility of Fgf8 is controversial. In the present study, having not detected androgen-inducible expression of Fgf8 in other mouse mammary cell lines or mouse prostate, we examined the Shionogi carcinoma 115-derived S115 cell line for mouse mammary tumor virus (MMTV) insertions or other nearby DNA rearrangements that might explain the androgen inducibility of Fgf8 in these cells. Southern blotting did not detect MMTV insertions near Fgf8 but did reveal a specific DNA rearrangement 3.7 kb upstream of Fgf8 in S115 cells and in other cells (SC115) independently derived from Shionogi carcinoma 115. Spectral karyotyping of S115 cells and sequencing of the cloned rearrangement junctions indicate that Fgf8 is involved in a t(5;19) translocation. The chromosome 5 sequence joined to Fgf8 is immediately adjacent to Smr2 (submaxillary gland androgen-regulated protein 2) and includes Muc10 (mucin 10), two genes that we show are testosterone inducible in S115 cells, suggesting that the androgen-dependent expression of Fgf8 in Shionogi carcinoma 115 and derivative cells results from this translocation. Together, these results suggest that androgen inducibility is not an inherent property of the Fgf8 gene, which has implications regarding this gene's proposed role in the etiology of hormone-responsive cancers.

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“…To activate these mechanisms, the mammary gland initiates a specific program to prepare the tissue to be a secretory organ for feeding the newborn. Therefore, several genes are turned on for the proliferation and differentiation of the mammary epithelium during the gestation period for the synthesis of nutrients to fulfill the requirements of the newborn (17)(18)(19)(20)(21).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of the sodium-coupled neutral amino acid transporter (SNAT2) by 17β-estradiol

Velázquez-Villegas

Ortíz

Ström

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The sodium-coupled neutral amino acid transporter 2 (SNAT2) translocates small neutral amino acids into the mammary gland to promote cell proliferation during gestation. It is known that SNAT2 expression increases during pregnancy, and in vitro studies indicate that this transporter is induced by 17β-estradiol. In this study, we elucidated the mechanism by which 17β-estradiol regulates the transcription of SNAT2. In silico analysis revealed the presence of a potential estrogen response element (ERE) in the SNAT2 promoter. Reporter assays showed an increase in SNAT2 promoter activity when cotransfected with estrogen receptor alpha (ER-α) after 17β-estradiol stimulation. Deletion of the ERE reduced estradiol-induced promoter activity by 63%. Additionally, EMSAs and supershift assays showed that ER-α binds to the SNAT2 ERE and that this binding competes with the interaction of ER-α with its consensus ERE. An in vivo ChIP assay demonstrated that the binding of ER-α to the SNAT2 promoter gradually increased in the mammary gland during gestation and that maximal binding occurred at the highest 17β-estradiol serum concentration. Liquid chromatography-elevated energy mass spectrometry and Western blot analysis revealed that the SNAT2 ER-α-ERE complex contained poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen protein p70, and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) proteins and that the silencing of each of these proteins nearly abolished 17β-estradiol-stimulated SNAT2 promoter activity. Nuclear levels of GAPDH increased progressively during gestation in the mammary gland, and GAPDH binding was nucleotide-specific for the SNAT2 ERE. Thus, this study provides new insights into how the mammary epithelium adapts to control amino acid uptake through the transcriptional regulation of the SNAT2 transporter via 17β-estradiol.coactivator | amino acid transport T he mammary gland has a high demand for amino acids during the gestation and lactation periods. It requires the uptake of amino acids for cell proliferation during pregnancy and for milk protein synthesis during lactation. Studies examining arteriovenous differences have demonstrated that glutamine and alanine are efficiently transported into the mammary gland at the start of lactation (1). These amino acids are primarily transported by amino acid transport system A, which is comprised of three subtypes known as sodium-coupled neutral amino acid transporter (SNAT) 1, 2, and 4 (2). SNAT2 is characterized as the classical system A transporter, is ubiquitous in mammalian cells, and plays various roles in different tissues and depending on specific physiological conditions (3-5). SNAT2 also provides efflux substrates for other amino acid transport systems, like the amino acid heteroexchanger system L, facilitating the uptake of branched-chain amino acids, particularly leucine that activates the TOR pathway involved in protein synthesis and cell proliferation (6). Up-regulation of SNAT2 gene expression is mediated by different signal transduction pathways. In the l...

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Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Cited by 32 publications

References 28 publications

Curcuminoid-phospholipid complex induces apoptosis in mammary epithelial cells by STAT-3 signaling

Curcuminoid-phospholipid complex induces apoptosis in mammary epithelial cells by STAT-3 signaling

Androgen inducibility of Fgf8 in Shionogi carcinoma 115 cells correlates with an adjacent t(5;19) translocation

Transcriptional regulation of the sodium-coupled neutral amino acid transporter (SNAT2) by 17β-estradiol

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