Epigenetic changes in cancer by Raman imaging, fluorescence imaging, AFM and scanning near-field optical microscopy (SNOM). Acetylation in normal and human cancer breast cells MCF10A, MCF7 and MDA-MB-231

The Analyst ◽  
2016 ◽  
Vol 141 (19) ◽  
pp. 5646-5658 ◽  
Author(s):  
Halina Abramczyk ◽  
Jakub Surmacki ◽  
Monika Kopeć ◽  
Alicja Klaudia Olejnik ◽  
Agnieszka Kaufman-Szymczyk ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Fluorescence Imaging ◽  
Breast Cancer Cells ◽  
Human Cancer ◽  
Near Field ◽  
Raman Imaging ◽  
Epigenetic Changes ◽  
Cancer Breast ◽  
Breast Cells

This paper examines epigenetic changes in breast cancer cells by Raman imaging, fluorescence imaging, AFM and SNOM.

scholarly journals Vascular endothelial growth factor encoded by Parapoxviruses can regulate metabolism and survival of triple negative breast cancer cells

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Dipayan Bose ◽  
Sagarika Banerjee ◽  
Rajnish Kumar Singh ◽  
Lyn M. Wise ◽  
Erle S. Robertson
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Normal Breast ◽  
Cancer Breast ◽  
Human Genes ◽  
Metabolic Gene Expression ◽  
Breast Cells

AbstractDysbiotic microbiomes are linked to many pathological outcomes including different metabolic disorders like diabetes, atherosclerosis and even cancer. Breast cancer is the second leading cause of cancer associated death in women, and triple negative breast cancer (TNBC) is the most aggressive type with major challenges for intervention. Previous reports suggested that Parapoxvirus signatures are one of the predominant dysbiotic viral signatures in TNBC. These viruses encode several genes that are homologs of human genes. In this study, we show that the VEGF homolog encoded by Parapoxviruses, can induce cell proliferation, and alter metabolism of breast cancer and normal breast cells, through alteration of MAPK-ERK and PI3K-AKT signaling. In addition, the activity of the transcription factor FoxO1 was altered by viral-encoded VEGF through activation of the PI3K-AKT pathway, leading to reprogramming of cellular metabolic gene expression. Therefore, this study provides new insights into the function of viral-encoded VEGFs, which promoted the growth of the breast cancer cells and imparted proliferative phenotype with altered metabolism in normal breast cells.

scholarly journals Arginine Methyltransferase PRMT1 Regulates p53 Activity in Breast Cancer

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 789
Author(s):  
Li-Ming Liu ◽  
Qiang Tang ◽  
Xin Hu ◽  
Jing-Jing Zhao ◽  
Yuan Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Asymmetric Dimethylarginine ◽  
Human Cancer ◽  
Specific Inhibitor ◽  
Dependent Manner ◽  
Breast Tumorigenesis ◽  
Stress Signals

The protein p53 is one of the most important tumor suppressors, responding to a variety of stress signals. Mutations in p53 occur in about half of human cancer cases, and dysregulation of the p53 function by epigenetic modifiers and modifications is prevalent in a large proportion of the remainder. PRMT1 is the main enzyme responsible for the generation of asymmetric-dimethylarginine, whose upregulation or aberrant splicing has been observed in many types of malignancies. Here, we demonstrate that p53 function is regulated by PRMT1 in breast cancer cells. PRMT1 knockdown activated the p53 signal pathway and induced cell growth-arrest and senescence. PRMT1 could directly bind to p53 and inhibit the transcriptional activity of p53 in an enzymatically dependent manner, resulting in a decrease in the expression levels of several key downstream targets of the p53 pathway. We were able to detect p53 asymmetric-dimethylarginine signals in breast cancer cells and breast cancer tissues from patients, and the signals could be significantly weakened by silencing of PRMT1 with shRNA, or inhibiting PRMT1 activity with a specific inhibitor. Furthermore, PRMT1 inhibitors significantly impeded cell growth and promoted cellular senescence in breast cancer cells and primary tumor cells. These results indicate an important role of PRMT1 in the regulation of p53 function in breast tumorigenesis.

scholarly journals Dual-Color Fluorescence Imaging of EpCAM and EGFR in Breast Cancer Cells with a Bull’s Eye-Type Plasmonic Chip

Sensors ◽  
2017 ◽  
Vol 17 (12) ◽  
pp. 2942 ◽  
Author(s):  
Shota Izumi ◽  
Shohei Yamamura ◽  
Naoko Hayashi ◽  
Mana Toma ◽  
Keiko Tawa
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Fluorescence Imaging ◽  
Breast Cancer Cells ◽  
Dual Color ◽  
Bull's Eye

scholarly journals Control of MYC-dependent apoptotic threshold by a co-amplified ubiquitin E3 ligase UBR5

2019 ◽  
Author(s):  
Xi Qiao ◽  
Ying Liu ◽  
Maria Llamazares Prada ◽  
Abhishekh Gupta ◽  
Alok Jaiswal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Ubiquitin Ligase ◽  
Breast Cancer Cells ◽  
Human Cancer ◽  
Cancer Therapeutics ◽  
Cancer Tissue ◽  
Basal Type

AbstractMYC protein expression has to be tightly controlled to allow for maximal cell proliferation without inducing apoptosis. Here we discover UBR5 as a novel MYC ubiquitin ligase and demonstrate how it functions as a molecular rheostat to prevent excess accumulation of MYC protein. UBR5 effects on MYC protein stability are independent on N-terminal FBW7 degron of MYC. Endogenous UBR5 inhibition induces MYC protein expression and activates MYC target genes. Moreover, UBR5 governs MYC-dependent phenotypes in vivo in Drosophila. In cancer cells, UBR5-mediated MYC protein suppression diminishes cell killing activity of cancer therapeutics. Further, we demonstrate that UBR5 dominates MYC protein expression at the single-cell level in human basal-type breast cancer tissue. Myc and Ubr5 are co-amplified in MYC-driven human cancer types, and UBR5 controls MYC-mediated apoptotic threshold in co-amplified basal type breast cancer cells. In summary, UBR5 is a novel MYC ubiquitin ligase and an endogenous rheostat for MYC protein expression in vivo. Clinically, expression of UBR5 may be important for protection of breast cancer cells from drug-induced, and MYC-dependent, apoptosis.

scholarly journals Extracellular vesicles from triple-negative breast cancer cells promote proliferation and drug resistance in non-tumorigenic breast cells

2018 ◽  
Vol 172 (3) ◽  
pp. 713-723 ◽  
Author(s):  
Patricia Midori Murobushi Ozawa ◽  
Faris Alkhilaiwi ◽  
Iglenir João Cavalli ◽  
Danielle Malheiros ◽  
Enilze Maria de Souza Fonseca Ribeiro ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Breast Cells

scholarly journals Breast-Associated Adipocytes Secretome Induce Fatty Acid Uptake and Invasiveness in Breast Cancer Cells via CD36 Independently of Body Mass Index, Menopausal Status and Mammary Density

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2012 ◽  
Author(s):  
Maurice Zaoui ◽  
Mehdi Morel ◽  
Nathalie Ferrand ◽  
Soraya Fellahi ◽  
Jean-Philippe Bastard ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Mass Index ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Body Mass ◽  
Breast Cancer Cells ◽  
Menopausal Status ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Breast Cells

Breast adiposity is correlated with body mass index, menopausal status and mammary density. We here wish to establish how these factors influence the cross-talk between breast adipocytes and normal or malignant breast cells. Adipocyte-derived stem cells (ASCs) were obtained from healthy women and classified into six distinct groups based on body mass index, menopausal status and mammary density. The ASCs were induced to differentiate, and the influence of their conditioned media (ACM) was determined. Unexpectedly, there were no detectable differences in adipogenic differentiation and secretion between the six ASC groups, while their corresponding ACMs had no detectable influence on normal breast cells. In clear contrast, all ACMs profoundly influenced the proliferation, migration and invasiveness of malignant breast cells and increased the number of lipid droplets in their cytoplasm via increased expression of the fatty acid receptor CD36, thereby increasing fatty acid uptake. Importantly, inhibition of CD36 reduced lipid droplet accumulation and attenuated the migration and invasion of the breast cancer cells. These findings suggest that breast-associated adipocytes potentiate the invasiveness of breast cancer cells which, at least in part, is mediated by metabolic reprogramming via CD36-mediated fatty acid uptake.

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