Breast cancer cell lines: friend or foe?

Burdall, S. E.; Hanby, Andrew M.; Lansdown, Mark; Speirs, Valerie

doi:10.1186/bcr577

Cited by 262 publications

(266 citation statements)

References 36 publications

(48 reference statements)

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“…This is particularly the case for microscopy studies, including large-scale siRNA screens with imaging read out. In contrast, there is substantial controversy of how well cell lines, which are often established from late stage cancer, preserve aspects of the disease and whether or not they should be used in cancer drug development (3)(4)(5). Thus animal experiments or studies in primary cell lines are often preferred despite their added complexity.…”

mentioning

confidence: 99%

Comparative Proteomic Phenotyping of Cell Lines and Primary Cells to Assess Preservation of Cell Type-specific Functions

Pan

Kumar

Böhl

et al. 2009

Molecular & Cellular Proteomics

436

313

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mentioning

confidence: 99%

Comparative Proteomic Phenotyping of Cell Lines and Primary Cells to Assess Preservation of Cell Type-specific Functions

Pan

Kumar

Böhl

et al. 2009

Molecular & Cellular Proteomics

436

313

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“…It is aggressive cancer cell line as it is not derived from the primary breast tumor; it is rather derived from the tumor which was metastasized [23]. On the other hand, the MC3T3 cell line was originally isolated for varying degrees of osteogenic potential and has been widely used as a normal non-cancerous model cell line in bone biology.…”

Section: Discussionmentioning

confidence: 99%

Dichloroacetic Acid (DCA)-Induced Cytotoxicity in Human Breast Cancer Cells Accompanies Changes in Mitochondrial Membrane Permeability and Production of Reactive Oxygen Species

Al-Karakooly¹,

Kilaparty²,

Al-Anbaky³

et al. 2014

JCT

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Cancer cells utilize cytosolic glycolysis for their energy production even in the presence of adequate levels of oxygen (Warbug effect) due to mitochondrial defects. Dichloroacetic acid (DCA) shifts cytosolic glucose metabolism to aerobic oxidation by inhibiting mitochondrial pyruvate dehydrogenase kinase (PDK) and increasing pyruvate uptake. Therefore, DCA has potential in reversing the glycolytic metabolism defect in cancerous cells. DCA is also known to induce apoptosis in a number of cancer cell lines, the mechanism of which is not well understood. In this study, an attempt has been made to investigate the effects of DCA on aggressive human breast cancer (MCF-7) cells as compared with less aggressive mouse osteoblastic (MC3T3) cells. Cell cytotoxicity was determined by MTT, crystal violet and Trypan blue exclusion assays. Western blot was used to detect any changes in the expression of apoptotic markers. Flow cytometry was used to measure apoptotic and necrotic effects of DCA. Mitochondrial integrity was determined by change in mitochondrial membrane potential (Δψm), whereas oxidative damage was determined by production * Corresponding author. Z. Alkarakooly et al. 1235of reactive oxygen species (ROS). DCA caused a concentration-dependent cytotoxicity both in MCF-7 and MC3T3 cell lines. MCF-7 cells were most affected. Flow cytometry results showed a significantly higher apoptosis in MCF-7 even at lower concentrations of DCA. However, higher concentrations of DCA were necrotic. Western blotting showed an increased expression of Mn-SOD-1 upon DCA treatment. Further, DCA decreased Δψm and increased ROS production. The effects of DCA were more pronounced on MCF-7 cells as compared to MC3T3 cells. Our results suggest that DCA-induced cytotoxicity in cancerous cells is mediated via changes in Δψm and production of ROS.

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“…MCF-7, and T47D are breast cancer epithelial cells derived from pleural effusions (36). MCF-10A is a normal breast epithelial cell line.…”

Section: Body Experimental Methodsmentioning

confidence: 99%

Consequences of Cyclin D1/BRCA1 Interaction in Breast Cancer Progression

Kehn¹,

Kashanchi²,

Bottazzi³

2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate The inheritance of one defective BRCA1 or BRCA2 allele predisposes an individual to developing breast, ovarian and T-cell cancers. In addition, in breast cancers where BRCAI is not mutated, it is often functionally inactivated. Furthermore, cyclin DI has been shown to be overexpressed in many cancers including breast cancer and its associates with BRCA1. Because of the crucial rold of both of these proteins in cancer, it is reasonable to expect that this interaction has a significant role in tumor cells. The understanding of when this interaction occurs during cell cycle progression will help to determine the role of cyclin D1/BRCAI binding in breast cancer cells. Therefore, I hypothesize that the direct interaction of cyclin D1 with BRCA1 results in the cell cycle dependent regulation of the activity ofBRCA1. In this study, I wish to identify and confirm the cell cycle dependent cyclin D1/BRCA1 interaction in breast cancer cells, determine the biochemical consequence of cyclin D1I/BRCA1 interaction in breast cancer cells, and determine the functional consequence of BRCAI phosphorylation in breast cancer. BRCAI's phosphorylation by cyclin DI/cdk complexes may help to regulate BRCAI's localization to the nucleus, since BRCAI has been shown to have a cytoplasmic expression pattern, but acts primarily in the nucleus. Phosphorylation may also be important in modulating BRCA1 's ability to bind DNA, either as a transcription factor or as part ofa DNA damage repair complex. Determining the consequences of the interaction of cyclin D1/BRCA1 could lead to a more complete understanding of how breast cancer occurs, thus leading to new treatment options.

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Breast cancer cell lines: friend or foe?

Cited by 262 publications

References 36 publications

Comparative Proteomic Phenotyping of Cell Lines and Primary Cells to Assess Preservation of Cell Type-specific Functions

Comparative Proteomic Phenotyping of Cell Lines and Primary Cells to Assess Preservation of Cell Type-specific Functions

Dichloroacetic Acid (DCA)-Induced Cytotoxicity in Human Breast Cancer Cells Accompanies Changes in Mitochondrial Membrane Permeability and Production of Reactive Oxygen Species

Consequences of Cyclin D1/BRCA1 Interaction in Breast Cancer Progression

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