Regulation of apoptosis in adipocytes and breast cancer cells by 1,25-dihydroxyvitamin D3: a link between obesity and breast cancer

2013 ◽  
Vol 14 (3) ◽  
Author(s):  
Igor N. Sergeev
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mammary Cancer ◽  
Tissue Mass ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Promising Strategy ◽  
Adipose Tissue Mass

AbstractModulation of apoptosis is emerging as a promising strategy for prevention and treatment of breast cancer and obesity because removal of mammary cancer cells and mature adipocytes through this process will result in decreasing tumor size and produce long-term reduction in adipose tissue mass. The hormone 1,25-dihydroxyvitamin D

Short- and long-term cytotoxic effects of doxorubicin conjugates with dendrimers and vector protein on MCF-7/MDR1 chemoresistant breast cancer cells

2017 ◽  
Author(s):  
I. A. Zamulaeva ◽  
O. N. Matchuk ◽  
K. A. Churyukina ◽  
V. A. Kudryavtzev ◽  
N. G. Yabbarov ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cytotoxic Effects ◽  
Short And Long Term ◽  
Mcf 7

Investigating Agents That Invoke Apoptotic Synergy of Long-Term Estrogen-Deprived Breast Cancer Cells

2011 ◽  
pp. P1-72-P1-72
Author(s):  
Sarah E Aiyar ◽  
Weitao Wang ◽  
Ji-ping Wang ◽  
Wei Yue ◽  
Richard J Santen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Growth factor–induced shedding of syndecan-1 confers glypican-1 dependence on mitogenic responses of cancer cells

2005 ◽  
Vol 171 (4) ◽  
pp. 729-738 ◽  
Author(s):  
Kan Ding ◽  
Martha Lopez-Burks ◽  
José Antonio Sánchez-Duran ◽  
Murray Korc ◽  
Arthur D. Lander
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cell Surface ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Sulfate Proteoglycan ◽  
Matrix Metalloproteinase 7 ◽  
Over Time

The cell surface heparan sulfate proteoglycan (HSPG) glypican-1 is up-regulated by pancreatic and breast cancer cells, and its removal renders such cells insensitive to many growth factors. We sought to explain why the cell surface HSPG syndecan-1, which is also up-regulated by these cells and is a known growth factor coreceptor, does not compensate for glypican-1 loss. We show that the initial responses of these cells to the growth factor FGF2 are not glypican dependent, but they become so over time as FGF2 induces shedding of syndecan-1. Manipulations that retain syndecan-1 on the cell surface make long-term FGF2 responses glypican independent, whereas those that trigger syndecan-1 shedding make initial FGF2 responses glypican dependent. We further show that syndecan-1 shedding is mediated by matrix metalloproteinase-7 (MMP7), which, being anchored to cells by HSPGs, also causes its own release in a complex with syndecan-1 ectodomains. These results support a specific role for shed syndecan-1 or MMP7–syndecan-1 complexes in tumor progression and add to accumulating evidence that syndecans and glypicans have nonequivalent functions in vivo.

scholarly journals Differential Response to 1,25-dihydroxyvitamin D in Metastatic and Non-Metastatic Breast Cancer Cell Lines in Hypoxia (P05-006-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Violet Kiesel ◽  
Stephen Hursting ◽  
Dorothy Teegarden
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Mammary Cancer ◽  
Metastatic Breast ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D

Abstract Objectives Prevention of metastasis is of utmost importance for increasing survival in breast cancer patients. Oxygen tension is variable throughout tumors, creating regions of hypoxia that have been linked with poor cancer prognosis. Hypoxia increases glycolytic flux via hypoxia-inducible factor-1α (HIF1α), and can therefore alter growth and survival of cancer cells. Our objectives are to (1) characterize changes in metabolism and survival that occur when metastatic and non-metastatic mammary cancer cell lines are cultured in hypoxia, and (2) determine whether 1,25-dihydroxyvitamin D (1,25(OH)2D) reduces overall survival in hypoxia. Methods We utilized Wnt oncogene-driven murine mammary cancer cells that are non-metastatic (M-Wnt) or that preferentially metastasize to the lung in vivo (metM-Wntlung). Viability of M-Wnt and metM-Wntlung cells treated with 10 nM 1,25(OH)2D and/or 20 mM 2-deoxyglucose (2DG, an inhibitor of glycolysis) was measured with MTT. Expression of HIF1α protein was determined by Western blotting. Results We show that 1,25(OH)2D treatment significantly decreased viability of metastatic metM-Wntlung cells grown in hypoxia by 41%, whereas viability of M-Wnt cells was not significantly impacted by 1,25(OH)2D treatment. Furthermore, treating cells with 2DG significantly decreased viability of both cells lines in hypoxia, with metM-Wntlung cells being more sensitive to 2DG. Interestingly, 1,25(OH)2D treatment partially rescued M-Wnt cells by 22% and metM-Wntlung cells by 24% when treated with 2DG in hypoxia. Finally, we show that M-Wnt cells have 1.9-fold increased expression of HIF1α protein compared to metM-Wntlung cells when grown in hypoxia. Conclusions Our results collectively suggest that non-metastatic M-Wnt cells are less sensitive to treatment with 1,25(OH)2D and 2DG in hypoxia than metastatic metM-Wntlungcells. These data may be explained, in part, by elevated expression of HIF1α in M-Wnt cells, which may contribute to their improved survival in hypoxia. Funding Sources National Institute of Health and USDA.

scholarly journals Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features

2016 ◽  
Vol 50 (1) ◽  
pp. 49-65 ◽  
Author(s):  
Robert Gelfand ◽  
Dolores Vernet ◽  
Kevin W. Bruhn ◽  
Suren Sarkissyan ◽  
David Heber ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mcf 7
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