scholarly journals Baicalin Promotes Mammary Gland Development via Steroid-Like Activities

2021 ◽  
Vol 9 ◽  
Author(s):  
Weizhen Chen ◽  
Wei Wei ◽  
Liya Yu ◽  
Xin Zhang ◽  
Fujing Huang ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Tumor Growth ◽  
Cell Line ◽  
Cancer Progression ◽  
Mammary Gland Development ◽  
Biological Activities ◽  
Xenograft Model ◽  
Mammary Development ◽  
Tumor Xenograft ◽  
Gland Development

Baicalin, the main flavonoid component extracted from Scutellaria roots, has a variety of biological activities and is therefore used in the treatment of many kinds of diseases. However, whether baicalin affects the normal development of tissues and organs is still unclear. Here, using a mouse mammary gland model, we investigated the effects of baicalin on the expansion of mammary stem cells (MaSCs) and mammary development, as well as breast cancer progression. Interestingly, we found that baicalin administration significantly accelerates duct elongation at puberty, and promotes alveolar development and facilitates milk secretion during pregnancy. Furthermore, self-renewal of MaSCs was significantly promoted in the presence of baicalin. Moreover, in a tumor xenograft model, baicalin promoted tumor growth of the MDA-MB-231 cell line, but suppressed tumor growth of the ZR-751 cell line. Mechanistically, baicalin can induce expression of the protein C receptor, while inhibiting the expression of the estrogen receptor. Transcriptome analysis revealed that baicalin is involved in signaling pathways related to mammary gland development, immune response, and cell cycle control. Taken together, our results from comprehensive investigation of the biological activity of baicalin provide a theoretical basis for its rational clinical application.

Targeting heparanase to the mammary epithelium enhances mammary gland development and promotes tumor growth and metastasis

2018 ◽  
Vol 65 ◽  
pp. 91-103 ◽  
Author(s):  
Ilanit Boyango ◽  
Uri Barash ◽  
Liat Fux ◽  
Inna Naroditsky ◽  
Neta Ilan ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Tumor Growth ◽  
Mammary Gland Development ◽  
Mammary Epithelium ◽  
Tumor Growth And Metastasis ◽  
Gland Development

scholarly journals A Functional Connection between pRB and Transforming Growth Factor β in Growth Inhibition and Mammary Gland Development

2009 ◽  
Vol 29 (16) ◽  
pp. 4455-4466 ◽  
Author(s):  
Sarah M. Francis ◽  
Jacqueline Bergsied ◽  
Christian E. Isaac ◽  
Courtney H. Coschi ◽  
Alison L. Martens ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Growth Factor ◽  
Growth Inhibition ◽  
Mammary Gland Development ◽  
Transforming Growth Factor ◽  
Critical Role ◽  
Transforming Growth Factor Β ◽  
Mammary Development ◽  
Functional Connection ◽  
Gland Development

ABSTRACT Transforming growth factor β (TGF-β) is a crucial mediator of breast development, and loss of TGF-β-induced growth arrest is a hallmark of breast cancer. TGF-β has been shown to inhibit cyclin-dependent kinase (CDK) activity, which leads to the accumulation of hypophosphorylated pRB. However, unlike other components of TGF-β cytostatic signaling, pRB is thought to be dispensable for mammary development. Using gene-targeted mice carrying subtle missense changes in pRB (Rb1 ΔL and Rb1NF ), we have discovered that pRB plays a critical role in mammary gland development. In particular, Rb1 mutant female mice have hyperplastic mammary epithelium and defects in nursing due to insensitivity to TGF-β growth inhibition. In contrast with previous studies that highlighted the inhibition of cyclin/CDK activity by TGF-β signaling, our experiments revealed that active transcriptional repression of E2F target genes by pRB downstream of CDKs is also a key component of TGF-β cytostatic signaling. Taken together, our work demonstrates a unique functional connection between pRB and TGF-β in growth control and mammary gland development.

scholarly journals Strain-Specific Differences in the Mechanisms of Progesterone Regulation of Murine Mammary Gland Development

Endocrinology ◽  
2008 ◽  
Vol 150 (3) ◽  
pp. 1485-1494 ◽  
Author(s):  
Mark D. Aupperlee ◽  
Alexis A. Drolet ◽  
Srinivasan Durairaj ◽  
Weizhong Wang ◽  
Richard C. Schwartz ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Mammary Gland Development ◽  
Nuclear Factor Κb ◽  
Mammary Development ◽  
Normal Mammary Gland ◽  
Human Populations ◽  
Induced Expression ◽  
Altered Expression ◽  
Downstream Effectors ◽  
Gland Development

Progesterone (P) is required for normal mammary gland development, and is implicated in the etiology of mammary cancer in rodents and humans. We analyzed mammary gland developmental responses to P and estrogen (E) in two strains of mice (BALB/c and C57BL/6) that exhibit differences in ductal development at sexual maturity and alveologenesis during pregnancy. C57BL/6 mice exhibited reduced proliferative and morphological responses to P. Analysis of known mediators of sidebranching and alveologenesis revealed that reduced P-induced expression of P receptor isoform B and receptor activator of nuclear factor-κB ligand (RANKL), as well as altered expression and regulation of cyclin D1, CCAAT/enhancer binding protein β, and the downstream effectors of RANKL, nuclear Id2 and p21, contribute significantly to the reduced P responsiveness of the C57BL/6 mammary gland. In contrast, E responsiveness was greater in C57BL/6 than in BALB/c glands. E may play a compensatory role in C57BL/6 alveologenesis through its effect on the induction and activation of signal transducer and activator of transcription 5a, a known regulator of RANKL. These observations suggest that in human populations with heterogeneous genetic backgrounds, individuals may respond differentially to the same hormone. Thus, genetic diversity may have a role in determining the effects of P in normal mammary development and tumorigenesis. Reduced progesterone-induced expression of progesterone receptor and RANKL, altered expression and regulation of C/EBPβ, and of the downstream effectors of RANKL, nuclear Id2 and p21, contribute significantly to the reduced progesterone-responsiveness of the C57BL/6 mammary gland compared to the BALB/c gland.

scholarly journals Food intake dependent and independent effects of heat stress on lactation and mammary gland development

2020 ◽  
Author(s):  
Yao Xiao ◽  
Jason M. Kronenfeld ◽  
Benjamin J. Renquist
Keyword(s):  
Heat Stress ◽  
Mammary Gland ◽  
Food Intake ◽  
Milk Production ◽  
Mammary Gland Development ◽  
Heat Exposure ◽  
Mammary Development ◽  
Late Gestation ◽  
Independent Effects ◽  
Gland Development

ABSTRACTWith a growing population, a reliable food supply is increasingly important. Heat stress reduces livestock meat and milk production. Genetic selection of high producing animals increases endogenous heat production, while climate change increases exogenous heat exposure. Both sources of heat exacerbate the risk of heat-induced depression of production. Rodents are valuable models to understand mechanisms conserved across species. Heat exposure suppresses feed intake across homeothermic species including rodents and production animal species. We assessed the response to early-mid lactation or late gestation heat exposure on milk production and mammary gland development/function, respectively. Using pair-fed controls we experimentally isolated the food intake dependent and independent effects of heat stress on mammary function and mass. Heat exposure (35°C, relative humidity 50%) decreased daily food intake. When heat exposure occurred during lactation, hypophagia accounted for approximately 50% of the heat stress induced hypogalactia. Heat exposure during middle to late gestation suppressed food intake, which was fully responsible for the lowered mammary gland weight of dams at parturition. However, the impaired mammary gland function in heat exposed dams measured by metabolic rate and lactogenesis could not be explained by depressed food consumption. In conclusion, mice recapitulate the depressed milk production and mammary gland development observed in dairy species while providing insight regarding the role of food intake. This opens the potential to apply genetic, experimental and pharmacological models unique to mice to identify the mechanism by which heat is limiting animal production.Summary StatementsThis study demonstrates that heat stress decreases lactation and mammary development through food intake dependent and independent mechanisms.

scholarly journals CD44 Promotes Epithelial Mammary Gland Development and Exhibits Altered Localization during Cancer Progression

2011 ◽  
Vol 2 (8) ◽  
pp. 771-781 ◽  
Author(s):  
J. M. V. Louderbough ◽  
J. A. Brown ◽  
R. B. Nagle ◽  
J. A. Schroeder
Keyword(s):  
Mammary Gland ◽  
Cancer Progression ◽  
Mammary Gland Development ◽  
Gland Development
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