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Review
. 2003 Dec;15(6):753-62.
doi: 10.1016/j.ceb.2003.10.016.

Tissue architecture: the ultimate regulator of breast epithelial function

Mina J Bissell  1 , Aylin Rizki, I Saira Mian
Affiliations
Review

Tissue architecture: the ultimate regulator of breast epithelial function

Mina J Bissell et al. Curr Opin Cell Biol. 2003 Dec.
No abstract available

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Figures

Figure 1
Figure 1
The mammary acinus as an experimental animal. Schematic presentation of a 3D acinus in basement membrane. Questions currently being addressed include the following. How is an acinus formed? How does it maintain polarity? How does it become disordered in malignancy? What molecules and signaling pathways are involved?
Figure 2
Figure 2
The structure resulting from acinus formation in 3D BM cultures resembles an in vivo mammary acinus [21]. (a) A low magnification transmission EM of an acinus formed in culture. (b) A light microscope picture of an acinus from a section of a gland in vivo.
Figure 3
Figure 3
Milk protein production requires a hierarchical set of events including availability of lactogenic hormones, correct cytoskeletal organization, laminin-1, proper cell–cell interactions, formation of acini with apico-basal polarity, and cavitation and formation of lumina for secretion of milk [33].
Figure 4
Figure 4
Myoepithelial cells contribute to correct polarity of luminal epithelial cell acini by providing laminin-1. Luminal epithelial cells make inside-out acini in collagen (middle) as shown by sialomucin (green) and ESA (red) staining. Addition of laminin-1 producing myoepithelial cells (MEP) to the 3D collagen cultures reverts the polarity (right) to resemble that of luminal epithelial cell acini in laminin-rich 3D BM (left) ([39•], reproduced with permission). Lr, laminin-rich.
Figure 5
Figure 5
Non-malignant and tumorigenic breast epithelial cells can be distinguished from each other in the 3D BM assay. HMT3522–T4-2 (tumorigenic) cells (middle panel) can be reverted to a near-normal morphology, as discussed in the text. Organization of F-actin (green) that is lost in T4-2 (tumor) cells (nuclei shown in red) is restored in T4-2 cells reverted by down-modulation of EGFR signaling [60] or other means (see Figure 6).
Figure 6
Figure 6
Reversion strategies as a means of understanding signaling integration in acini. (a) Up- or down-regulation of many factors can cause the reverted phenotype of T4-2 cells in 3D BM. (b) Many different cell lines, including metastatic cells, can be reverted by combination of the treatments shown in (a). (c) Venn diagram summarizing gene expression analysis of ~8000 genes using cDNA arrays. Genes that showed differential expression between T4-2 and reverted T4-2 cells when reversion was achieved either by β1-integrin blocking (left) or by EGFR down-regulation (right) are shown. Differentially expressed genes are defined as genes that show a p-value of 0.05 or lower in four experiments.
See this image and copyright information in PMC

References

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