Description

There are many different kinds of cells in the mammary glands. Since epithelial cells are the source of many human breast cancers and produce and secrete milk during lactation, they are the focus of numerous studies. Tissue culture research is the primary source of our understanding of the dynamic phases of tissue growth, function, and regression that characterize mammary gland biology. One of the most widely used in vitro scientific models is probably cell culture, and the two-dimensional culture system is still the most widely used research model. To improve the isolation, growth, yield, and viability of mammary gland cells, various methods and conditions have been tried and tested. The terms "cell culture," "mammary gland," and "human" were used in the search. Between July and August of 2021, two authors conducted the primary search. We also used a spreadsheet-based review matrix to organize and categorize information about each article for inclusion. The review included eleven studies that were the subject of qualitative analyses. Despite the fact that studies of these cells have been reported since the 1970s, the majority of those studies are from the past ten years and are largely carried out in the United States. In addition, the primary culture of Human Mammary Epithelial Cells (HMEC) obtained from breast surgery could be confirmed as the primary type of cell being studied.

Mammary Gland Tissue

Dulbecco's Modified Eagle Medium (DMEM) and M87A medium with various supplements are used to cultivate these cells. The use of dissociation reagents varied, and there was a dearth of information regarding cryopreservation. These study models' detailed methodological information has prompted us to suggest additional research. For adequate tissue development, maintenance, and regeneration, cell fate decisions are crucial. The microenvironment tightly controls the fates of epithelial cells in the mammary gland. During the development of the mammary gland, components of the microenvironment regulate cell fate decisions, and pathological changes in the microenvironment can alter cell fates, resulting in malignancy, are discussed in this section. In particular, we talk about the current understanding of three factors that control and direct the fate of mammary cells: hormones, the immune microenvironment, and the extracellular matrix—and how these components can combine to form microenvironments that support a fourth element: damage to DNA. Classes of noncoding RNAs known as circular RNAs are found in a lot of eukaryotic tissues and have been shown to have specific biological functions. An RNA sequencing method was used to compare the expression of circular RNAs in the mammary gland tissue of nine Small Tail Han sheep at the height of lactation and afterwards when they were not lactating because little is known about the function of circular RNAs in sheep mammary gland tissue.

The RNA from these nine sheep was pooled and analyzed in three lactation-peak and three non-lactation-peak libraries. Using reverse transcriptase-polymerase chain reaction and DNA sequencing, the expression and identity of nine of the 3,278 and 1,756 circular RNAs found in peak lactation and non-lactating mammary gland tissues, respectively, was confirmed. The type, location on the chromosome, and length of the circular RNAs that were found were determined. When compared to non-lactating mammary gland tissue, the peak lactation mammary gland tissue contained forty up-regulated and one down-regulated circular RNAs. These differentially expressed circular RNAs' parental genes had connections to molecular function, binding, protein binding, ATP binding, and ion binding, as determined by gene ontology enrichment analysis. In the constructed circular RNA–microRNA network, some microRNAs reportedly associated with the development of the mammary gland were found. Five differentially expressed circular RNAs were chosen for further analysis to predict their target microRNAs. This study provides a better understanding of the roles that circular RNAs play in sheep's mammary gland by revealing the expression profiles and characterization of circular RNAs at two crucial stages of activity. It is unclear how heterochromatin affects the selection of a cell's fate during development. De novo chromatin opening, abnormal formation of the mammary ductal tree, impaired stem cell potential, disrupted intraductal polarity, and loss of tissue function are all caused by the absence of H3K9 methyltransferase G9a in the mammary epithelium, as shown by our findings. Long Terminal Repeat (LTR) retroviral sequences, most notably the ERVK family, are depressed by G9a loss.

Mammary Morphological Defects

Double-stranded DNA (dsDNA) is produced by transcriptionally activated endogenous retroviruses, which elicits an antiviral innate immune response. In G9a knockout (G9acKO) mammary epithelium, the cytosolic dsDNA sensor Aim2 rescues mammary ductal invasion. The immune-compromised or G9acKO-conditioned host's mammary morphological defects are partially dependent on the inflammatory milieu of the host's mammary fat pad after mammary stem cell transplantation. As a result, both cell-autonomous and non-autonomous mechanisms disrupt mammary gland development and stem cell activity when retroviral elements' chromatin accessibility is altered. The formation of mammary placodes, the invagination of flask-shaped mammary buds, and the development of miniature bi-layered ductal trees are all part of the embryonic mammary gland development process. There is currently a good understanding of the factors that influence the movement of ectodermal cells to form these appendages and the pathways that lead to the specification and commitment of the mammary gland. Cell surface proteins and transcription factors that encourage the emergence of unipotent progenitors, as well as gene expression profiles of early populations of bipotent mammary stem cells, have been identified. Analyses of these populations have revealed parallel processes in breast cancer and embryonic mammary development. An overview of the highly conserved pathways that shape the embryonic mammary gland is provided in this section. Attempts to eradicate cancer by restoring differentiatent signals could benefit greatly from gaining an understanding of the dynamic signaling events that take place during normal mammary development. It has long been known that the stroma in the mammary gland plays a crucial role in controlling the development, function, and cancer of the mammary epithelium.

However, it has only recently begun to become clearer what each stromal cell population does. Through paracrine signaling, extracellular matrix production and remodeling, and regulation of other stromal cell types, mammary fibroblasts have emerged as master regulators and modulators of epithelial cell behavior. We provide a synopsis of the most important studies that shed light on the roles that fibroblasts play in the development of the mammary gland in this review article. In addition, we discuss the origin, diversity, and plasticity of mammary fibroblasts throughout the development of the mammary gland and the progression of cancer. Upregulation of Growth Hormone (GH) has been linked to breast cancer promotion and/or progression. GH plays a crucial role in the growth and development of the mammary gland. The morphological characteristics and expression of receptors involved in mammary growth, development, and cancer, as well as mitogenic mediators, were analyzed in the mammary gland of virgin adult transgenic mice that overexpress GH to determine how high GH levels could promote oncogenic transformation of mammary tissue. When compared to wild-type mice, whole mounting and histologic analysis revealed that transgenic mice lack branching, have fewer alveolar structures, and exhibit increased epithelial ductal elongation and enlarged ducts. In transgenic mice, there was a decrease in the number of differentiated alveolar structures, but there were no differences in the number of Terminal End Buds (TEBs) between the two groups of mice. Breast tissue from GH-overexpressing mice had higher levels of GH, Insulin-like Growth Factor 1 (IGF1), and GH receptor mRNA, as well as higher levels of IGF1 receptor protein. However, transgenic mice had lower levels of GH receptor protein. The progesterone receptor and the epidermal growth factor receptor, two essential receptors for breast development, were also found to be increased in transgenic animal mammary tissue. In turn, GH-overexpressing mice had elevated levels of the proliferation marker Ki67, cFOS, and Cyclin D1, but they did not have elevated levels of cJUN or cMYC. In conclusion, prolonged exposure to high GH levels alters the normal development of the mammary gland through morphological and molecular changes. Although these effects wouldn't necessarily be tumorigenic, they might make people more likely to transform into oncogenes.