scholarly journals Breast Cancer Metabolism and Mitochondrial Activity: The Possibility of Chemoprevention with Metformin

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Massimiliano Cazzaniga ◽  
Bernardo Bonanni

Metabolic reprogramming refers to the ability of cancer cells to alter their metabolism in order to support the increased energy request due to continuous growth, rapid proliferation, and other characteristics typical of neoplastic cells. It has long been believed that the increase of metabolic request was independent of the mitochondrial action but recently we know that mitochondrial activity together with metabolism plays a pivotal role in the regulation of the energy needed for tumor cell growth and proliferation. For these reasons the mitochondria pathways could be a new target for therapeutic and chemopreventive intervention. Metformin in particular is actually considered a promising agent against mitochondrial activity thanks to its ability to inhibit the mitochondrial complex I.

2019 ◽  
Vol 18 (8) ◽  
pp. e3041
Author(s):  
B. Schöpf ◽  
H. Weissensteiner ◽  
G. Schäfer ◽  
A. Naschberger ◽  
B. Rupp ◽  
...  

2019 ◽  
Vol 8 (12) ◽  
pp. 2184 ◽  
Author(s):  
Ivana Kurelac ◽  
Ander Abarrategi ◽  
Moira Ragazzi ◽  
Luisa Iommarini ◽  
Nikkitha Umesh Ganesh ◽  
...  

A cogent issue in cancer research is how to account for the effects of tumor microenvironment (TME) on the response to therapy, warranting the need to adopt adequate in vitro and in vivo models. This is particularly relevant in the development of strategies targeting cancer metabolism, as they will inevitably have systemic effects. For example, inhibition of mitochondrial complex I (CI), despite showing promising results as an anticancer approach, triggers TME-mediated survival mechanisms in subcutaneous osteosarcoma xenografts, a response that may vary according to whether the tumors are induced via subcutaneous injection or by intrabone orthotopic transplantation. Thus, with the aim to characterize the TME of CI-deficient tumors in a model that more faithfully represents osteosarcoma development, we set up a humanized bone niche ectopic graft. A prominent involvement of TME was revealed in CI-deficient tumors, characterized by the abundance of cancer associated fibroblasts, tumor associated macrophages and preservation of osteocytes and osteoblasts in the mineralized bone matrix. The pseudo-orthotopic approach allowed investigation of osteosarcoma progression in a bone-like microenvironment setting, without being invasive as the intrabone cell transplantation. Additionally, establishing osteosarcomas in a humanized bone niche model identified a peculiar association between targeting CI and bone tissue preservation.


2006 ◽  
Vol 14 (4) ◽  
pp. 1089-1094 ◽  
Author(s):  
Nadia Chahboune ◽  
Isabel Barrachina ◽  
Inmaculada Royo ◽  
Vanessa Romero ◽  
Jairo Sáez ◽  
...  

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