scholarly journals Int6 regulates both proteasomal degradation and translation initiation and is critical for proper formation of acini by human mammary epithelium

Oncogene ◽  
2010 ◽  
Vol 30 (6) ◽  
pp. 724-736 ◽  
Author(s):  
J Suo ◽  
S J Snider ◽  
G B Mills ◽  
C J Creighton ◽  
A C Chen ◽  
...  
Keyword(s):  
Translation Initiation ◽  
Mammary Epithelium ◽  
Proteasomal Degradation ◽  
Human Mammary Epithelium

scholarly journals Cloning of partial cDNA encoding differentiation and tumor-associated mucin glycoproteins expressed by human mammary epithelium.

1987 ◽  
Vol 84 (17) ◽  
pp. 6060-6064 ◽  
Author(s):  
S. J. Gendler ◽  
J. M. Burchell ◽  
T. Duhig ◽  
D. Lamport ◽  
R. White ◽  
...  
Keyword(s):  
Mammary Epithelium ◽  
Mucin Glycoproteins ◽  
Human Mammary Epithelium ◽  
Partial Cdna

scholarly journals Normal breast epithelial MCF-10A cells to evaluate the safety of carbon dots

2021 ◽  
Author(s):  
Nuno Vale ◽  
Sara Silva ◽  
Diana Duarte ◽  
Diana M. A. Crista ◽  
Luís Pinto da Silva ◽  
...  
Keyword(s):  
Cell Line ◽  
Carbon Dots ◽  
Mammary Epithelium ◽  
Structural Similarity ◽  
Normal Breast ◽  
Breast Cell Line ◽  
Toxicity Studies ◽  
Human Mammary Epithelium ◽  
Normal Human ◽  
Breast Epithelial

The human normal breast cell line MCF-10A is being widely used as a model in toxicity studies due to its structural similarity to the normal human mammary epithelium.

scholarly journals Aldehyde dehydrogenase and estrogen receptor define a hierarchy of cellular differentiation in the normal human mammary epithelium

2014 ◽  
Vol 16 (3) ◽  
Author(s):  
Gabriella Honeth ◽  
Sara Lombardi ◽  
Christophe Ginestier ◽  
Minhee Hur ◽  
Rebecca Marlow ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Aldehyde Dehydrogenase ◽  
Cellular Differentiation ◽  
Mammary Epithelium ◽  
Human Mammary Epithelium ◽  
Normal Human

scholarly journals Oncogenic mutation or overexpression of oncogenic KRAS or BRAF is not sufficient to confer oncogene addiction

2020 ◽  
Author(s):  
Reina E. Ito ◽  
Chitose Oneyama ◽  
Kazuhiro Aoki
Keyword(s):  
Cancer Cells ◽  
Mammary Epithelium ◽  
Oncogene Addiction ◽  
Oncogenic Mutation ◽  
Tumorigenic Potential ◽  
Human Mammary Epithelium ◽  
Single Allele ◽  
Tumorigenic Activity ◽  
Cellular Property ◽  
Synthetic Biology Approach

AbstractOncogene addiction is a cellular property by which cancer cells become highly dependent on the expression of oncogenes for their survival. Oncogene addiction can be exploited to design molecularly targeted drugs that kill only cancer cells by inhibiting the specific oncogenes. Genes and cell lines exhibiting oncogene addiction, as well as the mechanisms by which cell death is induced when addicted oncogenes are suppressed, have been extensively studied. However, it is still not fully understood how oncogene addiction is acquired in cancer cells. Here, we take a synthetic biology approach to investigate whether oncogenic mutation or oncogene expression suffices to confer the property of oncogene addiction to cancer cells. We employed human mammary epithelium-derived MCF-10A cells expressing the oncogenic KRAS or BRAF. MCF-10A cells harboring an oncogenic mutation in a single-allele of KRAS or BRAF showed weak tumorigenic activity, but no characteristics of oncogene addiction. MCF-10A cells overexpressing oncogenic KRAS demonstrated the tumorigenic activity, but MCF-10A cells overexpressing oncogenic BRAF did not. Neither cell line exhibited any oncogene addiction properties. These results indicate that the introduction of oncogenic mutation or the overexpression of oncogenes is not sufficient for cancer cells to acquire oncogene addiction, and that oncogene addiction is not associated with tumorigenic potential.

scholarly journals RAL GTPases mediate EGFR-driven intestinal stem cell proliferation and tumourigenesis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Máté Nászai ◽  
Karen Bellec ◽  
Yachuan Yu ◽  
Alvaro Román-Fernández ◽  
Emma Sandilands ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Mapk Pathway ◽  
Mammary Epithelium ◽  
Intestinal Stem Cell ◽  
Stem Cell Proliferation ◽  
Pathway Activation ◽  
Ral Gtpases ◽  
Human Mammary Epithelium ◽  
Stem And Progenitor Cells

RAS-like (RAL) GTPases function in Wnt signalling-dependent intestinal stem cell proliferation and regeneration. Whether RAL proteins work as canonical RAS effectors in the intestine, and the mechanisms of how they contribute to tumourigenesis remain unclear. Here, we show that RAL GTPases are necessary and sufficient to activate EGFR/MAPK signalling in the intestine, via induction of EGFR internalisation. Knocking down Drosophila RalA from intestinal stem and progenitor cells leads to increased levels of plasma membrane-associated EGFR and decreased MAPK pathway activation. Importantly, in addition to impacting stem cell proliferation during damage-induced intestinal regeneration, this role of RAL GTPases impacts on EGFR-dependent tumorigenic growth in the intestine and in human mammary epithelium. However, the effect of oncogenic RAS in the intestine is independent from RAL function. Altogether, our results reveal previously unrecognised cellular and molecular contexts where RAL GTPases become essential mediators of adult tissue homeostasis and malignant transformation.

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