scholarly journals High Capacity of the Metastatic Breast Tumor Cells in Sphere Formation: Clue for Chemoresistance in TripleNegative Breast Cancer

2020 ◽  
Author(s):  
mohammad kamalabadi farahani
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Breast Tumor ◽  
High Capacity ◽  
Metastatic Breast ◽  
Breast Tumor Cells ◽  
Sphere Formation ◽  
Metastatic Breast Tumor

scholarly journals Biochemical and Anti-Triple Negative Metastatic Breast Tumor Cell Properties of Psammaplins

Marine Drugs ◽  
2018 ◽  
Vol 16 (11) ◽  
pp. 442 ◽  
Author(s):  
Yu-Dong Zhou ◽  
Jun Li ◽  
Lin Du ◽  
Fakhri Mahdi ◽  
Thuy Le ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Triple Negative ◽  
Hdac Inhibitors ◽  
Metastatic Breast ◽  
Dependent Manner ◽  
Breast Tumor Cells ◽  
Metastatic Breast Tumor

Breast tumors reprogram their cellular metabolism, nutrient uptake, and utilization-associated biochemical processes. These processes become further transformed as genetically predisposed metastatic breast tumor cells colonize specific organs. Breast tumor cells often metastasize to the brain, bone, lung and liver. Massagué and colleagues isolated organotropic subclones and established organ-specific gene signatures associated with lung-, bone-, and brain-specific metastatic triple-negative breast cancer (TNBC) MDA-MB-231 cells. Using these genetically characterized metastatic subclones specific to lung (LM4175), bone (BoM1833), and brain (BrM-2a), we evaluated marine natural products for the ability to differentially suppress metastatic breast cancer cells in a target organ-dependent manner. Psammaplin-based histone deacetylase (HDAC) inhibitors were found to differentially inhibit HDAC activity, induce activation of hypoxia-inducible factor-1 (HIF-1), and disrupt organotropic metastatic TNBC subclone growth. Further, psammaplins distinctly suppressed the outgrowth of BoM1833 tumor spheroids in 3D-culture systems. Similar results were observed with the prototypical HDAC inhibitor trichostatin A (TSA). These organotropic tumor cell-based studies suggest the potential application of HDAC inhibitors that may yield new directions for anti-metastatic breast tumor research and drug discovery.

scholarly journals E-cadherin re-expression shows in vivo evidence for mesenchymal to epithelial transition in clonal metastatic breast tumor cells

Oncotarget ◽  
2016 ◽  
Vol 7 (28) ◽  
pp. 43363-43375 ◽  
Author(s):  
Katie Palen ◽  
James Weber ◽  
Michael B. Dwinell ◽  
Bryon D. Johnson ◽  
Ramani Ramchandran ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Metastatic Breast ◽  
Breast Tumor Cells ◽  
Mesenchymal To Epithelial Transition ◽  
Metastatic Breast Tumor ◽  
E Cadherin

scholarly journals Non-overlapping activities of ADF and cofilin-1 during the migration of metastatic breast tumor cells

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
Lubna H Tahtamouni ◽  
Alisa E Shaw ◽  
Maram H Hasan ◽  
Salem R Yasin ◽  
James R Bamburg
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Metastatic Breast ◽  
Breast Tumor Cells ◽  
Metastatic Breast Tumor

Bone-derived soluble factors and laminin-511 cooperate to promote migration, invasion and survival of bone-metastatic breast tumor cells

2014 ◽  
Vol 32 (2) ◽  
pp. 63-73 ◽  
Author(s):  
Delphine Denoyer ◽  
Nicole Kusuma ◽  
Allan Burrows ◽  
Xiawei Ling ◽  
Lara Jupp ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Metastatic Breast ◽  
Soluble Factors ◽  
Breast Tumor Cells ◽  
Metastatic Breast Tumor

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

scholarly journals RIPK3 upregulation confers robust proliferation and collateral cystine-dependence on breast cancer recurrence

2019 ◽  
Author(s):  
Chao-Chieh Lin ◽  
Nathaniel Mabe ◽  
Yi-Tzu Lin ◽  
Wen-Hsuan Yang ◽  
Xiaohu Tang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Tumor Recurrence ◽  
Cancer Recurrence ◽  
Breast Cancer Recurrence ◽  
Recurrent Tumor ◽  
Breast Tumor Cells ◽  
Recurrent Tumors ◽  
Recurrent Breast

AbstractThe molecular and genetic basis of tumor recurrence is complex and poorly understood. RIPK3 is a key effector in programmed necrotic cell death and, therefore, its expression is frequently suppressed in primary tumors. In a transcriptome profiling between primary and recurrent breast tumor cells from a murine model of breast cancer recurrence, we found that RIPK3, while absent in primary tumor cells, is dramatically re-expressed in recurrent breast tumor cells by an epigenetic mechanism. Unexpectedly, we found that RIPK3 knockdown in recurrent tumor cells reduced clonogenic growth, causing cytokinesis failure, p53 stabilization, and repressed the activities of YAP/TAZ. These data uncover a surprising role of the pro-necroptotic RIPK3 kinase in enabling productive cell cycle during tumor recurrence. Remarkably, high RIPK3 expression also rendered recurrent tumor cells exquisitely dependent on extracellular cystine and undergo programmed necrosis upon cystine deprivation. The induction of RIPK3 in recurrent tumors unravels an unexpected mechanism that paradoxically confers on tumors both growth advantage and necrotic vulnerability, providing potential strategies to eradicate recurrent tumors.

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