Regulation of Mammary Epithelial Cell Growth in Mice and Rats*

Imagawa, Walter; Bandyopadhyay, Gautam; Nandi, Satyabrata

doi:10.1210/edrv-11-4-494

Cited by 199 publications

(102 citation statements)

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“…1 Processes such as ductal morphogenesis, lobulo-alveolar development during pregnancy and lactation and involution are characterized by different degrees of apoptosis and proliferation. 2,3 These biological mechanisms are controlled by an interplay of hormones, growth factors, cell-cell and cell-matrix interactions.…”

Section: Introductionmentioning

confidence: 99%

“…4 One of the locally-derived growth factor families that has been implicated in these processes is the epidermal growth factor (EGF) family. 1,5 Both EGF and transforming growth factor-a (TGF-a) can stimulate the proliferation of mammary epithelial cells and lobulo-alveolar development in the mammary gland of virgin mice. 1,6 These growth factors are also able to modulate milk protein expression in mammary epithelial cells when cells are exposed to lactogenic hormones 7 and can inhibit apoptosis in secretory alveolar epithelial cells in the involuting mammary gland when ectopically overexpressed.…”

Section: Introductionmentioning

confidence: 99%

“…1,5 Both EGF and transforming growth factor-a (TGF-a) can stimulate the proliferation of mammary epithelial cells and lobulo-alveolar development in the mammary gland of virgin mice. 1,6 These growth factors are also able to modulate milk protein expression in mammary epithelial cells when cells are exposed to lactogenic hormones 7 and can inhibit apoptosis in secretory alveolar epithelial cells in the involuting mammary gland when ectopically overexpressed. 8 We recently identified another EGF-related protein, CR-1 (cripto-1) that can also modulate mammary epithelial cell morphogenesis and differentiation.…”

Section: Introductionmentioning

confidence: 99%

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Cripto-1 induces apoptosis in HC-11 mouse mammary epithelial cells

Santis

Martínez-Lacaci²,

Bianco³

et al. 2000

Cell Death Differ

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Cripto-1 (CR-1) is an epidermal growth factor (EGF)-related protein. CR-1 can inhibit b-casein and whey acidic protein expression in mouse mammary epithelial cells. The present study demonstrates that CR-1 can induce apoptosis in HC-11 mouse mammary epithelial cells, as measured by bisbenzimide stained nuclei, TUNEL assay and cell death ELISA. Apoptosis could be observed after 2 days of exposure of confluent HC-11 cells to CR-1 in the absence of the survival factors EGF and insulin, with maximum apoptosis occurring at 3 days. A reduction in poly(ADP-ribose) polymerase (PARP) expression and an increase in b-catenin cleavage was found after 18 h of exposure to CR-1 suggesting that apoptosis was preceded by the induction of a caspase activity since the caspase inhibitor ZFAD.FMK could block the CR-1-induced reduction in PARP expression and CR-1-induced apoptosis. CR-1 was found to increase the expression of caspase-3-like protease. Although, the levels of p27 kip1 and p21Bax did not change after exposure to CR-1 for 18 h, the levels of Bcl-x L became undetectable. These studies suggest that CR-1 promotes apoptosis by mediating the induction of caspase-3-like protease and downregulating the expression of Bcl-x L .

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cripto-1 induces apoptosis in HC-11 mouse mammary epithelial cells

Santis

Martínez-Lacaci²,

Bianco³

et al. 2000

Cell Death Differ

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“…LiCl, a potent mitogen for mammary epithelial cells (22,23), has been found to alter the phosphatidylinositol hydrolysis in MECs. Although LiCl also modulates the cAMP synthesis, K+ and Ca2+ transport, and guanine nucleotide-binding protein synthesis in other cell types, the exact mechanism of its mitogenic effect is still unclear (1). Using an expression cloning system, we have cloned and sequenced the gene,$ and our data indicate that overexpression is the possible mode of activation of the transforming gene.…”

mentioning

confidence: 95%

“…Hormones from ovaries and pituitary glands are absolutely essential for the proliferation and differentiation of mammary epithelial cells (MECs), which are the predominant carcinogen-susceptible cell type in the mammary gland (1). Studies from several laboratories have indicated that hormones play a crucial role in chemical carcinogen-induced mammary tumorigenesis in both mouse and rat model systems (2)(3)(4)(5).…”

mentioning

confidence: 99%

Identification of a mammary transforming gene (MAT1) associated with mouse mammary carcinogenesis.

Bera

Guzman

Miyamoto

et al. 1994

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

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We have developed an eent in vitro transformation system using N-methyl-N-nitrosourea that aflows us to study the role of hormones and growth factors in mouse mammary tumorigenesis. Ulizing this system, we reported earlier that mammary tumors induced in vitro with N-methyl-N-nitrosourea in the presence of mamogenic hormones (progesterone and prolactin) contain predominately an activated c-Ki-ras protooncogene with a G35 --A35 transitional mutation in the 12th codon. Mammary tumors induced in the presence of another mitogen, lithium (Li), do not have a mutation in the c-Ki-ras protooncogene. By using an expression cloning system, a pl d cone containing a 1. transversion mutations at the 61st codon of the H-ras protooncogene (9-12). A majority ofthymic lymphomas induced with MNU, on the other hand, contain a G35 --A35 mutation in the N-ras protooncogene (13,14).The long-term goal of our laboratory is to understand the role of mammogenic hormones and related growth factors in the growth and differentiation of MECs and the manner in which these factors influence the induction of mammary neoplasias of different phenotypes and genotypes. To achieve our goal, during the past several years we have developed a defined serum-free cell culture system in which mouse MECs embedded in a three-dimensional collagen gel matrix can be grown, induced to differentiate, and be neoplastically transformed with chemical carcinogens (15). Using this system, we have observed that the types of mammary lesions induced by carcinogens are greatly influenced by the mitogens present around the time of carcinogen treatment. Earlier we reported on an in vitro system for the induction of preneoplastic hyperplastic alveolar nodules (HANs) and carcinomas from MECs exposed to the direct-acting chemical carcinogen MNU in the presence of different mitogens (16). When mouse MECs were grown in the presence of the mammogenic hormones progesterone and prolactin (PPRL) during MNU administration, the predominant types of lesions induced were a high incidence ofHANs and carcinomas with squamous metaplasia. In contrast, when epidermal growth factor was used as a mitogen during the carcinogen treatment, only a low incidence of ductal hyperplasia was detected, although the extent of MEC proliferation between the two groups was equivalent. The genetic analysis of these lesions indicated that the activation ofthe protooncogene was also dependent on the mitogen used around the time of carcinogen treatment. The majority (80%o) of the HANs and carcinomas induced with MNU in the presence of PPRL had an activation ofthe protooncogene c-Ki-ras by a specific G35 -* A35 point mutation at codon 12. The activation of the protooncogene was determined to be an early event in this carcinogenesis process because the activation was detected in preneoplastic lesions (17). In contrast, activation of c-Kiras was absent in all the ductal hyperplasias induced by MNU in the presence of the mitogen epidermal growth factor. Involvement of the same type of c-Ki-ras mutation ha...

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Adenosine-mediated inhibition of casein production by mouse mammary glands in culture

et al. 1996

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The present study was carried out to examine whether activation of adenosine receptors by adenosine analogues will affect casein production by mouse mammary epithelial cells. The morphogenesis and functions of epithelial tissue in the mammary gland are influenced by their surrounding adipocytes. Adipocytes are known to release adenosine into the extracellular fluid which can modulate cyclic-AMP levels in surrounding cells through binding to their adenosine receptors. To examine a possible paracrine effect of adenosine, the modulation of casein production in mammary explant culture and mammary epithelial cell (MEC) culture by adenosine receptor agonists has been investigated. We have observed that activation of the A1-adenosine receptor subtype in mammary tissue by an adenosine analogue (-)N6-(R-phenyl-isopropyl)-adenosine (PIA) raised cAMP levels. PIA and another adenosine receptor agonist, isobutylmethylxanthine (IBMX), inhibited casein accumulation both in explants and in MEC cultures in the presence of lactogenic hormones, which suggests that PIA or adenosine can act directly on the epithelial cells. This inhibition does not appear to be caused by elevation of cAMP levels or phosphodiesterase activity. The inhibition of intracellular casein accumulation by PIA and IBMX in explant cultures can be reversed via treatment of pertussis toxin which is known to ADP-ribosylate GTP-binding G alpha i-proteins, indicating that a Gi-protein-dependent pathway may be involved in this inhibition. The results also suggest that local accumulation of adenosine in the extracellular fluids of mammary glands is likely to inhibit the lactogenic response of mammary epithelial cells.

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Regulation of Mammary Epithelial Cell Growth in Mice and Rats*

Cited by 199 publications

References 0 publications

Cripto-1 induces apoptosis in HC-11 mouse mammary epithelial cells

Cripto-1 induces apoptosis in HC-11 mouse mammary epithelial cells

Identification of a mammary transforming gene (MAT1) associated with mouse mammary carcinogenesis.

Adenosine-mediated inhibition of casein production by mouse mammary glands in culture

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