Metabolic Reorganization in Breast Cancer Epithelial Cells: Role of the Pentose Phosphate Shunt

2011 ◽  
Author(s):  
Susan Frost
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Pentose Phosphate ◽  
Pentose Phosphate Shunt

Metabolic Reorganization in Breast Cancer Epithelial Cells: Role of the Pentose Phosphate Shunt

2009 ◽  
Author(s):  
Susan C. Frost ◽  
Art Edison ◽  
Nick Simpson
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Pentose Phosphate ◽  
Pentose Phosphate Shunt

scholarly journals Mammary gland adipocytes in lactation cycle, obesity and breast cancer

2021 ◽  
Author(s):  
Georgia Colleluori ◽  
Jessica Perugini ◽  
Giorgio Barbatelli ◽  
Saverio Cinti
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Close Association ◽  
Critical Role ◽  
Exocrine Gland ◽  
Plastic Properties ◽  
Lactation Cycle ◽  
Gland Development

AbstractThe mammary gland (MG) is an exocrine gland present in female mammals responsible for the production and secretion of milk during the process of lactation. It is mainly composed by epithelial cells and adipocytes. Among the features that make the MG unique there are 1) its highly plastic properties displayed during pregnancy, lactation and involution (all steps belonging to the lactation cycle) and 2) its requirement to grow in close association with adipocytes which are absolutely necessary to ensure MG’s proper development at puberty and remodeling during the lactation cycle. Although MG adipocytes play such a critical role for the gland development, most of the studies have focused on its epithelial component only, leaving the role of the neighboring adipocytes largely unexplored. In this review we aim to describe evidences regarding MG’s adipocytes role and properties in physiologic conditions (gland development and lactation cycle), obesity and breast cancer, emphasizing the existing gaps in the literature which deserve further investigation.

scholarly journals Metabolome Shift in Both Metastatic Breast Cancer Cells and Astrocytes Which May Contribute to the Tumor Microenvironment

2021 ◽  
Vol 22 (14) ◽  
pp. 7430
Author(s):  
Hiromi Sato ◽  
Ayaka Shimizu ◽  
Toya Okawa ◽  
Miaki Uzu ◽  
Momoko Goto ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Metastatic Breast ◽  
Principal Component ◽  
Pentose Phosphate ◽  
Metastatic Brain Tumors ◽  
Pentose Phosphate Pathways ◽  
Culture Supernatants

The role of astrocytes in the periphery of metastatic brain tumors is unclear. Since astrocytes regulate central nervous metabolism, we hypothesized that changes in astrocytes induced by contact with cancer cells would appear in the metabolome of both cells and contribute to malignant transformation. Coculture of astrocytes with breast cancer cell supernatants altered glutamate (Glu)-centered arginine–proline metabolism. Similarly, the metabolome of cancer cells was also altered by astrocyte culture supernatants, and the changes were further amplified in astrocytes exposed to Glu. Inhibition of Glu uptake in astrocytes reduces the variability in cancer cells. Principal component analysis of the cancer cells revealed that all these changes were in the first principal component (PC1) axis, where the responsible metabolites were involved in the metabolism of the arginine–proline, pyrimidine, and pentose phosphate pathways. The contribution of these changes to the tumor microenvironment needs to be further pursued.

Role of Sphk1 in the malignant transformation of breast epithelial cells and breast cancer progression

2014 ◽  
Vol 51 (4) ◽  
pp. 524 ◽  
Author(s):  
Y Zhang ◽  
J Jiang ◽  
XD Zheng ◽  
Y Zhang ◽  
XW Qi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Malignant Transformation ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Breast Epithelial Cells ◽  
Breast Epithelial

scholarly journals The role of iodine and δ-iodolactone in growth and apoptosis of malignant thyroid epithelial cells and breast cancer cells

HORMONES ◽  
2010 ◽  
Vol 9 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Roland Gärtner ◽  
Petra Rank ◽  
Birgit Ander
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells

Maintenance of cellular NADPH is critical to intestinal cell survival during oxidative challenge: Role of glucose and pentose phosphate shunt activity

2003 ◽  
Vol 124 (4) ◽  
pp. A601
Author(s):  
Sarah Stringer ◽  
Carol A. Rhoads ◽  
Alex Ekshyyan ◽  
Laura Coe ◽  
Tak Yee Aw
Keyword(s):  
Cell Survival ◽  
Pentose Phosphate ◽  
Intestinal Cell ◽  
Oxidative Challenge ◽  
Pentose Phosphate Shunt

scholarly journals NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways

2020 ◽  
Author(s):  
Lin Cao ◽  
Xin Wang ◽  
Juhong Yang ◽  
Jia Guo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Functional Role ◽  
Polysialic Acid ◽  
Breast Epithelial Cells ◽  
Differential Signaling ◽  
Breast Epithelial

Abstract Background Neural cell adhesion molecule (NCAM), a common mammalian cell surface glycoprotein, is the major substrate of polysialic acid (PSA). Polysialylated NCAM occurs in many types of cancer, but rarely in normal adult tissues. Epithelial-mesenchymal transition (EMT) is an important process contributing to tumor metastasis. The functional role of NCAM hypersialylation in EMT is unclear. Method Expression of NCAM and PSA-NCAM in breast cancer progression were evaluated by western blot (WB), immunohistochemistry, semi-quantitative PCR and immunoprecipitation (IP). Overexpression of NCAM-140 and STX were performed to assess the functional role of NCAM hypersialylation by liposome transfection. Then, the cell proliferation ability was investigated with MTT assay. Transwell and wound closure assay were conducted to evaluate cell migratory ability. Phagokinetic gold sol assay and cell adhesion assay were performed to assess cell motility ability and cell adhesion ability, respectively. Furthermore, WB and IP were used to reveal the activated signaling pathway. Results The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways, based on the following observations: (i) NCAM and PSA-NCAM were aberrantly regulated in breast cancer cells; (ii) NCAM and PSA-NCAM expression were upregulated in normal breast epithelial cells undergoing EMT; (iii) NCAM overexpression induced EMT in breast epithelial cells; (iv) NCAM promoted cell proliferation and migration through activation of a β-catenin/slug signaling pathway; (v) modification of PSA attached to NCAM inhibited cell adhesion and promoted cell motility through activation of an EGFR/STAT3 pathway. Conclusion These observations help clarify the molecular mechanisms whereby PSA and its major substrate NCAM modulate cell behaviors, and the significance of increased PSA expression on NCAM during EMT and tumor development.

scholarly journals Role of the Microenvironment in Regulating Normal and Cancer Stem Cell Activity: Implications for Breast Cancer Progression and Therapy Response

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1240 ◽  
Author(s):  
Vasudeva Bhat ◽  
Alison L. Allan ◽  
Afshin Raouf
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Epithelial Cells ◽  
Cancer Stem Cells ◽  
Breast Tissue ◽  
Therapy Response ◽  
Breast Epithelial Cells ◽  
Tissue Microenvironment ◽  
Breast Epithelial

The epithelial cells in an adult woman’s breast tissue are continuously replaced throughout their reproductive life during pregnancy and estrus cycles. Such extensive epithelial cell turnover is governed by the primitive mammary stem cells (MaSCs) that proliferate and differentiate into bipotential and lineage-restricted progenitors that ultimately generate the mature breast epithelial cells. These cellular processes are orchestrated by tightly-regulated paracrine signals and crosstalk between breast epithelial cells and their tissue microenvironment. However, current evidence suggests that alterations to the communication between MaSCs, epithelial progenitors and their microenvironment plays an important role in breast carcinogenesis. In this article, we review the current knowledge regarding the role of the breast tissue microenvironment in regulating the special functions of normal and cancer stem cells. Understanding the crosstalk between MaSCs and their microenvironment will provide new insights into how an altered breast tissue microenvironment could contribute to breast cancer development, progression and therapy response and the implications of this for the development of novel therapeutic strategies to target cancer stem cells.

scholarly journals NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways

2020 ◽  
Author(s):  
Lin Cao ◽  
Xin Wang ◽  
Juhong Yang ◽  
Jia Guo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Functional Role ◽  
Polysialic Acid ◽  
Breast Epithelial Cells ◽  
Differential Signaling ◽  
Breast Epithelial

Abstract Background Neural cell adhesion molecule (NCAM), a common mammalian cell surface glycoprotein, is the major substrate of polysialic acid (polySia). Polysialylated NCAM occurs in many types of cancer, but rarely in normal adult tissues. Epithelial-mesenchymal transition (EMT) is an important process contributing to tumor metastasis. The functional role of NCAM hypersialylation in EMT is unclear. Method Expression of NCAM and polysialylated NCAM in breast cancer progression were evaluated by western blot (WB), immunohistochemistry, semi-quantitative PCR and immunoprecipitation (IP). Overexpression of NCAM-140 and ST8SiaII were performed to assess the functional role of NCAM hypersialylation by liposome transfection. Cell proliferation ability was investigated with MTT assay. Transwell and wound closure assay were conducted to evaluate cell migratory ability. Phagokinetic gold sol assay and cell adhesion assay were performed to assess cell motility ability and cell adhesion ability, respectively. Furthermore, WB and IP were used to reveal the activated signaling pathway. Results The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways, based on the following observations: (i) NCAM and polysialylated NCAM were aberrantly regulated in breast cancer cells; (ii) NCAM and polysialylated NCAM expression were upregulated in normal breast epithelial cells undergoing EMT; (iii) NCAM overexpression induced EMT in breast epithelial cells; (iv) NCAM promoted cell proliferation and migration through activation of a β-catenin/slug signaling pathway; (v) modification of polySia attached to NCAM inhibited cell adhesion and promoted cell motility through activation of an EGFR/STAT3 pathway. Conclusion This study demonstrates that NCAM and polysialylated NCAM facilitate different signaling pathway and affect different cell behaviors. Switching between the NCAM-mediated pathways appeared to depend on polySia decoration.

scholarly journals Endotoxin Triggers Tumor Initiation Events in Nontumorigenic Breast Epithelial Cells and Enhances Invasion-Related Phenotype in Pretumorigenic and Tumorigenic Breast Epithelial Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Farah Yassine ◽  
Sabreen F. Fostok ◽  
Nataly Naser Al Deen ◽  
Rabih S. Talhouk
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Human Breast ◽  
Short Term ◽  
Breast Epithelial Cells ◽  
Inflammatory Phenotype ◽  
Breast Cells ◽  
Breast Epithelial

Inflammation is associated with the development of several cancers, including breast cancer. However, the molecular mechanisms driving breast cancer initiation or enhancement by inflammation are yet to be deciphered. Hence, we opted to investigate the role of inflammation in initiating and enhancing tumor-like phenotypes in nontumorigenic, pretumorigenic, and tumorigenic breast epithelial cells. Noncytotoxic endotoxin (ET) concentrations capable of inducing an inflammatory phenotype were determined for the different cell lines. Results showed that short-term ET exposure upregulated matrix metalloproteinase-9 (MMP-9) activity in nontumorigenic mammary epithelial cells of mouse (SCp2) and human origins (HMT-3522 S1; S1) and upregulated inflammatory mediators including nitric oxide (NO) and interleukin 1-β in tumorigenic human breast cells (MDA-MB-231), all in a dose-dependent manner. Long-term ET treatment, but not short-term, triggered the migration of SCp2 cells, and proliferation and migration of tumorigenic human breast cells MCF-7 and MDA-MB-231. Both short- and long-term ET exposures preferentially enhanced the invasion of pretumorigenic S1-connexin 43 knockout (Cx43-KO S1) cells compared to their nontumorigenic S1 counterparts. Moreover, both ET exposures disrupted lumen formation and apicolateral distribution of β-catenin in 3D cultures of S1 cells. In conclusion, ET treatment at concentrations that elicited inflammatory phenotype triggered tumor initiation events in nontumorigenic and pretumorigenic breast cells, and increased tumorigenicity of breast cancer cells. Our findings highlight the role of inflammation in enhancing migration, invasion, and loss of normal 3D morphology and suggest that such inflammatory insults can “add injury” to pretumorigenic and tumorigenic breast epithelial cells.

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