scholarly journals ERβ alters the chemosensitivity of luminal breast cancer cells by regulating p53 function

Oncotarget ◽  
2018 ◽  
Vol 9 (32) ◽  
pp. 22509-22522 ◽  
Author(s):  
Igor Bado ◽  
Eric Pham ◽  
Benjamin Soibam ◽  
Fotis Nikolos ◽  
Jan-Åke Gustafsson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luminal Breast Cancer

scholarly journals Decreased LRIG1 in fulvestrant-treated luminal breast cancer cells permits ErbB3 upregulation and increased growth

Oncogene ◽  
2015 ◽  
Vol 35 (9) ◽  
pp. 1143-1152 ◽  
Author(s):  
M M Morrison ◽  
M M Williams ◽  
D B Vaught ◽  
D Hicks ◽  
J Lim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luminal Breast Cancer

scholarly journals Erratum: Decreased LRIG1 in fulvestrant-treated luminal breast cancer cells permits ErbB3 upregulation and increased growth

Oncogene ◽  
2016 ◽  
Vol 35 (9) ◽  
pp. 1206-1206 ◽  
Author(s):  
M M Morrison ◽  
M M Williams ◽  
D B Vaught ◽  
D Hicks ◽  
J Lim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luminal Breast Cancer

scholarly journals Dermatan Sulfate Affects Breast Cancer Cell Function via the Induction of Necroptosis

Cells ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 173
Author(s):  
Grzegorz Wisowski ◽  
Adam Pudełko ◽  
Krystyna Olczyk ◽  
Monika Paul-Samojedny ◽  
Ewa M. Koźma
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cell Function ◽  
Dermatan Sulfate ◽  
Variable Structure ◽  
Structural Features ◽  
Luminal Breast Cancer ◽  
Binding Properties

Dermatan sulfate (DS) is widespread in the extracellular matrix (ECM) of animal tissues. This glycosaminoglycan is characterized by a variable structure, which is reflected in the heterogeneity of its sulfation pattern. The sulfate groups are responsible for the binding properties of DS, which determine an interaction profile of this glycan. However, the detailed role of DS in biological processes such as the neoplasm is still poorly understood. The aim of the study was to assess the effects of the structural variants of DS on breast cancer cells. We found that DS isoforms from normal and fibrotic fascia as well as from intestinal mucosa were able to quickly induce oxidative stress in the cytoplasm and affect the mitochondrial function in luminal breast cancer cells. Moreover, the variants caused the necroptosis of the cells most likely via the first of these mechanisms. This death was responsible for a reduction in the viability and number of breast cancer cells. However, the dynamics and intensity of all of the DS variants-triggered effects were strongly dependent on the cell type and the structure of these molecules. The most pronounced activity was demonstrated by those variants that shared structural features with the DS from the tumor niche.

scholarly journals AXL Controls Directed Migration of Mesenchymal Triple-Negative Breast Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 247 ◽  
Author(s):  
Olivier Zajac ◽  
Renaud Leclere ◽  
André Nicolas ◽  
Didier Meseure ◽  
Caterina Marchiò ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Golgi Apparatus ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Leading Edge ◽  
Luminal Breast Cancer ◽  
Directed Migration

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with high risk of relapse and metastasis. TNBC is a heterogeneous disease comprising different molecular subtypes including those with mesenchymal features. The tyrosine kinase AXL is expressed in mesenchymal cells and plays a role in drug resistance, migration and metastasis. We confirm that AXL is more expressed in mesenchymal TNBC cells compared to luminal breast cancer cells, and that its invalidation impairs cell migration while having no or little effect on cell viability. Here, we found that AXL controls directed migration. We observed that AXL displays a polarized localization at the Golgi apparatus and the leading edge of migratory mesenchymal TNBC cells. AXL co-localizes with F-actin at the front of the cells. In migratory polarized cells, the specific AXL inhibitor R428 displaces AXL and F-actin from the leading edge to a lateral area localized between the front and the rear of the cells where both are enriched in protrusions. In addition, R428 treatment disrupts the polarized localization of the Golgi apparatus towards the leading edge in migratory cells. Immunohistochemical analysis of aggressive chemo-resistant TNBC samples obtained before treatment reveals inter- and intra-tumor heterogeneity of the percentage of AXL expressing tumor cells, and a preference of these cells to be in contact with the stroma. Taken together, our study demonstrates that AXL controls directed cell migration most likely by regulating cell polarity.

scholarly journals piRNA-823 Is Involved in Cancer Stem Cell Regulation Through Altering DNA Methylation in Association With Luminal Breast Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Xin Ding ◽  
Ya Li ◽  
Jinhui Lü ◽  
Qian Zhao ◽  
Yuefan Guo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Stem Cell ◽  
Cancer Cells ◽  
Cancer Biology ◽  
Breast Cancer Cells ◽  
Dna Methyltransferases ◽  
Luminal Breast Cancer ◽  
Stem Cell Markers ◽  
Luminal Subtype

Cancer stem cells (CSCs) are believed to be the main source of cancer relapse and metastasis. PIWI-interacting small non-coding RNAs (piRNAs) have been recently recognized to be relevant to cancer biology. Whether and how piRNAs regulate human CSCs remain unknown. Herein, upregulation of piR-823 was identified in tested luminal breast cancer cells, especially in the luminal subtype of breast CSCs. Enforced expression or targeted knockdown of piR-823 demonstrated its oncogenic function in regulating cell proliferation and colony formation in MCF-7 and T-47D breast cancer cells. In addition, piR-823 induced ALDH (+) breast CSC subpopulation promoted the expression of stem cell markers including OCT4, SOX2, KLF4, NANOG, and hTERT, and increased mammosphere formation. Tail vein injection of magnetic nanoparticles carrying anti-piR-823 into the mammary gland of tumor-burdened mice significantly inhibited tumor growth in vivo. DNA methyltransferases (DNMTs) including DNMT1, DNMT3A, and DNMT3B were demonstrated to be the downstream genes of piR-823, which regulate gene expression by maintaining DNA methylation. piR-823 increased the expression of DNMTs, promoted DNA methylation of gene adenomatous polyposis coli (APC), thereby activating Wnt signaling and inducing cancer cell stemness in the luminal subtype of breast cancer cells. The current study not only revealed a novel mechanism through which piRNAs contribute to tumorigenesis in breast cancer by regulating CSCs, but also provided a therapeutic strategy using non-coding genomes in the suppression of human breast cancer.

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