Development of a new diagnostic Raman method for monitoring epigenetic modifications in the cancer cells of human breast tissue

2016 ◽  
Vol 8 (48) ◽  
pp. 8542-8553 ◽  
Author(s):  
Beata Brozek-Pluska ◽  
Monika Kopeć ◽  
Halina Abramczyk
Keyword(s):  
Cancer Cells ◽  
Breast Tissue ◽  
Epigenetic Modifications ◽  
Raman Imaging ◽  
Human Breast ◽  
Human Breast Tissue

Raman imaging can ‘upgrade’ cancer epigenetic tests and answer many questions by monitoring the biochemistry of cancer cells.

scholarly journals Everolimus induces G1 cell cycle arrest through autophagy-mediated protein degradation of cyclin D1 in breast cancer cells

2019 ◽  
Vol 317 (2) ◽  
pp. C244-C252 ◽  
Author(s):  
Guang Chen ◽  
Xiao-Fei Ding ◽  
Hakim Bouamar ◽  
Kyle Pressley ◽  
Lu-Zhe Sun
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Breast Tissue ◽  
Human Breast ◽  
Human Breast Tissue ◽  
Cycle Arrest

Everolimus inhibits mammalian target of rapamycin complex 1 (mTORC1) and is known to cause induction of autophagy and G1 cell cycle arrest. However, it remains unknown whether everolimus-induced autophagy plays a critical role in its regulation of the cell cycle. We, for the first time, suggested that everolimus could stimulate autophagy-mediated cyclin D1 degradation in breast cancer cells. Everolimus-induced cyclin D1 degradation through the autophagy pathway was investigated in MCF-10DCIS.COM and MCF-7 cell lines upon autophagy inhibitor treatment using Western blot assay. Everolimus-stimulated autophagy and decrease in cyclin D1 were also tested in explant human breast tissue. Inhibiting mTORC1 with everolimus rapidly increased cyclin D1 degradation, whereas 3-methyladenine, chloroquine, and bafilomycin A1, the classic autophagy inhibitors, could attenuate everolimus-induced cyclin D1 degradation. Similarly, knockdown of autophagy-related 7 (Atg-7) also repressed everolimus-triggered cyclin D1 degradation. In addition, everolimus-induced autophagy occurred earlier than everolimus-induced G1 arrest, and blockade of autophagy attenuated everolimus-induced G1 arrest. We also found that everolimus stimulated autophagy and decreased cyclin D1 levels in explant human breast tissue. These data support the conclusion that the autophagy induced by everolimus in human mammary epithelial cells appears to cause cyclin D1 degradation resulting in G1 cell cycle arrest. Our findings contribute to our knowledge of the interplay between autophagy and cell cycle regulation mediated by mTORC1 signaling and cyclin D1 regulation.

scholarly journals Quantifying Breast Cancer-Driven Fiber Alignment and Collagen Deposition in Primary Human Breast Tissue

2021 ◽  
Vol 9 ◽  
Author(s):  
Rakesh Gurrala ◽  
C. Ethan Byrne ◽  
Loren M. Brown ◽  
Rafael Felix P. Tiongco ◽  
Margarite D. Matossian ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Tissue ◽  
Breast Tumors ◽  
Collagen Deposition ◽  
Human Breast ◽  
Human Breast Tissue ◽  
Fiber Alignment ◽  
Primary Human Breast

Solid tumor progression is significantly influenced by interactions between cancer cells and the surrounding extracellular matrix (ECM). Specifically, the cancer cell-driven changes to ECM fiber alignment and collagen deposition impact tumor growth and metastasis. Current methods of quantifying these processes are incomplete, require simple or artificial matrixes, rely on uncommon imaging techniques, preclude the use of biological and technical replicates, require destruction of the tissue, or are prone to segmentation errors. We present a set of methodological solutions to these shortcomings that were developed to quantify these processes in cultured, ex vivo human breast tissue under the influence of breast cancer cells and allow for the study of ECM in primary breast tumors. Herein, we describe a method of quantifying fiber alignment that can analyze complex native ECM from scanning electron micrographs that does not preclude the use of replicates and a high-throughput mechanism of quantifying collagen content that is non-destructive. The use of these methods accurately recapitulated cancer cell-driven changes in fiber alignment and collagen deposition observed by visual inspection. Additionally, these methods successfully identified increased fiber alignment in primary human breast tumors when compared to human breast tissue and increased collagen deposition in lobular breast cancer when compared to ductal breast cancer. The successful quantification of fiber alignment and collagen deposition using these methods encourages their use for future studies of ECM dysregulation in human solid tumors.

Human T47D-ERβ breast cancer cells with tetracycline-dependent ERβ expression reflect ERα/ERβ ratios in rat and human breast tissue

2013 ◽  
Vol 27 (6) ◽  
pp. 1753-1761 ◽  
Author(s):  
N.M. Evers ◽  
T.M.C. van de Klundert ◽  
Y.M. van Aesch ◽  
S. Wang ◽  
W.K. de Roos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Breast Tissue ◽  
Human Breast ◽  
Human Breast Tissue

Phase Transitions in Oleic Acid and in Human Breast Tissue As Studied by Raman Spectroscopy and Raman Imaging

2011 ◽  
Vol 54 (9) ◽  
pp. 3386-3392 ◽  
Author(s):  
Beata Brozek-Pluska ◽  
Joanna Jablonska-Gajewicz ◽  
Radzislaw Kordek ◽  
Halina Abramczyk
Keyword(s):  
Raman Spectroscopy ◽  
Oleic Acid ◽  
Phase Transitions ◽  
Breast Tissue ◽  
Raman Imaging ◽  
Human Breast ◽  
Human Breast Tissue

Effects of oestrogen on gene expression in epithelium and stroma of normal human breast tissue

2006 ◽  
Vol 13 (2) ◽  
pp. 617-628 ◽  
Author(s):  
C L Wilson ◽  
A H Sims ◽  
A Howell ◽  
C J Miller ◽  
R B Clarke
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Proliferation ◽  
Breast Tissue ◽  
Epithelial Cell Proliferation ◽  
Human Breast ◽  
Human Breast Tissue ◽  
Tissue Microenvironment ◽  
Normal Human Breast ◽  
Normal Human

Oestrogen (E) is essential for normal and cancer development in the breast, while anti-oestrogens have been shown to reduce the risk of the disease. However, little is known about the effect of E on gene expression in the normal human breast, particularly when the epithelium and stroma are intact. Previous expression profiles of the response to E have been performed on tumour cell lines, in the absence of stroma. We investigated gene expression in normal human breast tissue transplanted into 9–10-week-old female athymic nude (Balb/c nu/nu) mice. After 2 weeks, when epithelial proliferation is minimal, one-third of the mice were treated with 17β-oestradiol (E2) to give human luteal-phase levels in the mouse, which we have previously shown to induce maximal epithelial cell proliferation. RNA was isolated from treated and untreated mice, labelled and hybridized to Affymetrix HG-U133A (human) GeneChips. Gene expression levels were generated using BioConductor implementations of the RMA and MAS5 algorithms. E2 treatment was found to represent the largest source of variation in gene expression and cross-species hybridization of mouse RNA from xenograft samples was demonstrated to be negligible. Known E2-responsive genes (such as TFF1 and AREG), and genes thought to be involved in breast cancer metastasis (including mammoglobin, KRT19 and AGR2), were upregulated in response to E treatment. Genes known to be co-expressed with E receptor α in breast cancer cell lines and tumours were both upregulated (XBP-1 and GREB1) and downregulated (RARRES1 and GATA3). In addition, genes that are normally expressed in the myoepithelium and extracellular matrix that maintain the tissue microenvironment were also differentially expressed. This suggests that the response to oestrogen in normal breast is highly dependent upon epithelial–stromal/myoepithelial interactions which maintain the tissue microenvironment during epithelial cell proliferation.

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