scholarly journals Cross-Talk of Breast Cancer Cells with the Immune System

10.5772/22545 ◽  
2011 ◽  
Author(s):  
Sandra Demaria ◽  
Karsten A. ◽  
Sylvia Adams
Keyword(s):  
Breast Cancer ◽  
Immune System ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells

scholarly journals Stimulatory Cross-talk between NFAT3 and Estrogen Receptor in Breast Cancer Cells

2005 ◽  
Vol 280 (52) ◽  
pp. 43188-43197 ◽  
Author(s):  
Hao Zhang ◽  
Xiangyang Xie ◽  
Xudong Zhu ◽  
Jianhua Zhu ◽  
Chunfang Hao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells

Cross-Talk Between Notch and EGFR Signaling in Human Breast Cancer Cells

2009 ◽  
Vol 27 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Jianjian Dai ◽  
Daoxin Ma ◽  
Shaolei Zang ◽  
Dongmei Guo ◽  
Xun Qu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cross Talk ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Egfr Signaling ◽  
Human Breast

scholarly journals Interplay Between Mitophagy and Apoptosis Defines a Cell Fate Upon Co-treatment of Breast Cancer Cells With a Recombinant Fragment of Human κ-Casein and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand

2021 ◽  
Vol 8 ◽  
Author(s):  
Fabian Wohlfromm ◽  
Max Richter ◽  
Lado Otrin ◽  
Kamil Seyrek ◽  
Tanja Vidaković-Koch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells ◽  
Tumor Necrosis ◽  
Short Term ◽  
Recombinant Fragment ◽  
Necrosis Factor

A recombinant fragment of human κ-Casein, termed RL2, induces cell death of breast cancer cells; however, molecular mechanisms of RL2-mediated cell death have remained largely unknown. In the current study, we have decoded the molecular mechanism of the RL2-mediated cell death and found that RL2 acts via the induction of mitophagy. This was monitored by the loss of adenosine triphosphate production, LC3B-II generation, and upregulation of BNIP3 and BNIP3L/NIX, as well as phosphatase and tensin homolog-induced kinase 1. Moreover, we have analyzed the cross talk of this pathway with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis upon combinatorial treatment with RL2 and TRAIL. Strikingly, we found two opposite effects of this co-treatment. RL2 had inhibitory effects on TRAIL-induced cell death upon short-term co-stimulation. In particular, RL2 treatment blocked TRAIL-mediated caspase activation, cell viability loss, and apoptosis, which was mediated via the downregulation of the core proapoptotic regulators. Contrary to short-term co-treatment, upon long-term co-stimulation, RL2 sensitized the cells toward TRAIL-induced cell death; the latter observation provides the basis for the development of therapeutic approaches in breast cancer cells. Collectively, our findings have important implications for cancer therapy and reveal the molecular switches of the cross talk between RL2-induced mitophagy and TRAIL-mediated apoptosis.

scholarly journals Prolactin Receptor–Integrin Cross-Talk Mediated by SIRPα in Breast Cancer Cells

2010 ◽  
Vol 8 (10) ◽  
pp. 1413-1424 ◽  
Author(s):  
Traci Galbaugh ◽  
Yvonne B. Feeney ◽  
Charles V. Clevenger
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells ◽  
Prolactin Receptor

BMP9 regulates cross-talk between breast cancer cells and bone marrow-derived mesenchymal stem cells

2014 ◽  
Vol 37 (5) ◽  
pp. 363-375 ◽  
Author(s):  
Shaoheng Wan ◽  
Yuehong Liu ◽  
Yaguang Weng ◽  
Wei Wang ◽  
Wei Ren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells

Breast cancer metabolic cross-talk: Fibroblasts are hubs and breast cancer cells are gatherers of lipids

2018 ◽  
Vol 462 ◽  
pp. 93-106 ◽  
Author(s):  
Filipa Lopes-Coelho ◽  
Saudade André ◽  
Ana Félix ◽  
Jacinta Serpa
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cross Talk ◽  
Breast Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document