scholarly journals Nuclear factor-ĸB plays a critical role in both intrinsic and acquired resistance against endocrine therapy in human breast cancer cells

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Kumiko Oida ◽  
Akira Matsuda ◽  
Kyungsook Jung ◽  
Yan Xia ◽  
Hyosun Jang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Endocrine Therapy ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Critical Role ◽  
Acquired Resistance ◽  
Nuclear Factor ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Iron metabolism disturbances in the MCF-7 human breast cancer cells with acquired resistance to doxorubicin and cisplatin

2013 ◽  
Vol 43 (5) ◽  
pp. 1481-1486 ◽  
Author(s):  
VASYL F. CHEKHUN ◽  
NATALIA Yu. LUKYANOVA ◽  
ANATOLIY P. BURLAKA ◽  
NATALIA A. BEZDENEZHNYKH ◽  
SVITLANA I. SHPYLEVA ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Iron Metabolism ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Acquired Resistance ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Resistance To Doxorubicin ◽  
Mcf 7

scholarly journals Hypoxia-inducible factor 1-dependent expression of adenosine receptor 2B promotes breast cancer stem cell enrichment

2018 ◽  
Vol 115 (41) ◽  
pp. E9640-E9648 ◽  
Author(s):  
Jie Lan ◽  
Haiquan Lu ◽  
Debangshu Samanta ◽  
Shaima Salman ◽  
You Lu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Adenosine Receptor ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Critical Role ◽  
Hypoxia Inducible Factor ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Hypoxia Inducible Factor 1

Breast cancer stem cells (BCSCs), which are characterized by a capacity for unlimited self-renewal and for generation of the bulk cancer cell population, play a critical role in cancer relapse and metastasis. Hypoxia is a common feature of the cancer microenvironment that stimulates the specification and maintenance of BCSCs. In this study, we found that hypoxia increased expression of adenosine receptor 2B (A2BR) in human breast cancer cells through the transcriptional activity of hypoxia-inducible factor 1. The binding of adenosine to A2BR promoted BCSC enrichment by activating protein kinase C-δ, which phosphorylated and activated the transcription factor STAT3, leading to increased expression of interleukin 6 and NANOG, two key mediators of the BCSC phenotype. Genetic or pharmacological inhibition of A2BR expression or activity decreased hypoxia- or adenosine-induced BCSC enrichment in vitro, and dramatically impaired tumor initiation and lung metastasis after implantation of MDA-MB-231 human breast cancer cells into the mammary fat pad of immunodeficient mice. These data provide evidence that targeting A2BR might be an effective strategy to eradicate BCSCs.

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