Mitochondrial reactive oxygen species and cancer
Abstract
Mitochondria produce reactive oxygen species (mROS) as a natural by-product of electron transport chain activity. While initial studies focused on the damaging effects of reactive oxygen species, a recent paradigm shift has shown that mROS can act as signaling molecules to activate pro-growth responses. Cancer cells have long been observed to have increased production of ROS relative to normal cells, although the implications of this increase were not always clear. This is especially interesting considering cancer cells often also induce expression of antioxidant proteins. Here, we discuss how ...
Source: Cancer and Metabolism - November 28, 2014 Category: Cancer & Oncology Source Type: research
The 2014 Beatson International Cancer Conference: Powering the Cancer Machine
Abstract
Here, we present a report of the 2014 annual Beatson International Cancer Conference, Glasgow, July 6–9, 2014. The theme was “Powering the Cancer Machine”, focusing on oncogenic signals that regulate metabolic rewiring and the adaptability of the metabolic network in response to stress. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - November 28, 2014 Category: Cancer & Oncology Source Type: research
Erratum to: Loss of HSulf-1 promotes altered lipid metabolism in ovarian cancer
(Source: Cancer and Metabolism)
Source: Cancer and Metabolism - November 4, 2014 Category: Cancer & Oncology Source Type: research
Metabolic and transcriptional profiling reveals pyruvate dehydrogenase kinase 4 as a mediator of epithelial-mesenchymal transition and drug resistance in tumor cells
Conclusions
Together, these findings implicate PDK4 as a critical metabolic regulator of EMT and associated drug resistance. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - November 3, 2014 Category: Cancer & Oncology Source Type: research
SIRT3 and SIRT4 are mitochondrial tumor suppressor proteins that connect mitochondrial metabolism and carcinogenesis
Abstract
It is a well-established scientific observation that mammalian cells contain fidelity proteins that appear to protect against and adapt to various forms of endogenous and exogenous cellular conditions. Loss of function or genetic mutation of these fidelity proteins has also been shown to create a cellular environment that is permissive for the development of tumors, suggesting that these proteins also function as tumor suppressors (TSs). While the first identified TSs were confined to either the nucleus and/or the cytoplasm, it seemed logical to hypothesize that the mitochondria may also contai...
Source: Cancer and Metabolism - October 20, 2014 Category: Cancer & Oncology Source Type: research
Putting the pieces together: How is the mitochondrial pathway of apoptosis regulated in cancer and chemotherapy?
Abstract
In order to solve a jigsaw puzzle, one must first have the complete picture to logically connect the pieces. However, in cancer biology, we are still gaining an understanding of all the signaling pathways that promote tumorigenesis and how these pathways can be pharmacologically manipulated by conventional and targeted therapies. Despite not having complete knowledge of the mechanisms that cause cancer, the signaling networks responsible for cancer are becoming clearer, and this information is serving as a solid foundation for the development of rationally designed therapies. One goal of chemot...
Source: Cancer and Metabolism - October 6, 2014 Category: Cancer & Oncology Source Type: research
Erratum to: Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia
(Source: Cancer and Metabolism)
Source: Cancer and Metabolism - September 29, 2014 Category: Cancer & Oncology Source Type: research
Endothelial cell metabolism: parallels and divergences with cancer cell metabolism
Abstract
The stromal vasculature in tumors is a vital conduit of nutrients and oxygen for cancer cells. To date, the vast majority of studies have focused on unraveling the genetic basis of vessel sprouting (also termed angiogenesis). In contrast to the widely studied changes in cancer cell metabolism, insight in the metabolic regulation of angiogenesis is only just emerging. These studies show that metabolic pathways in endothelial cells (ECs) importantly regulate angiogenesis in conjunction with genetic signals. In this review, we will highlight these emerging insights in EC metabolism and discuss the...
Source: Cancer and Metabolism - September 15, 2014 Category: Cancer & Oncology Source Type: research
Q&A: targeting autophagy in cancer—a new therapeutic?
Abstract
Macroautophagy (autophagy hereafter) captures and degrades intracellular proteins and organelles in lysosomes as a quality control mechanism and recycles their components to sustain survival in starvation. Cellular self-cannibalization by autophagy is thought to have a context-dependent role in cancer. Autophagy inactivation is destructive to normal tissues and can promote cancer initiation while some established cancers upregulate autophagy that promotes their survival. We are only beginning to understand the role of autophagy in cancer and the precise mechanisms behind tumour suppression and ...
Source: Cancer and Metabolism - September 11, 2014 Category: Cancer & Oncology Source Type: research
Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia
Conclusions
Thus, our studies demonstrate that the cachectic phenotype is in part due to metabolic alterations in tumor cells, which can be reverted by a ketogenic diet, causing reduced tumor growth and inhibition of muscle and body weight loss. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - September 1, 2014 Category: Cancer & Oncology Source Type: research
Metformin directly acts on mitochondria to alter cellular bioenergetics
Conclusions
Together, these results demonstrate that metformin directly acts on mitochondria to limit respiration and that the sensitivity of cells to metformin is dependent on their ability to cope with energetic stress. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - August 28, 2014 Category: Cancer & Oncology Source Type: research
Loss of HSulf-1 promotes altered lipid metabolism in ovarian cancer
Conclusions
Taken together, these findings demonstrate that loss of HSulf-1 potentially contributes to the metabolic alterations associated with the progression of ovarian pathogenesis, specifically impacting the lipogenic phenotype of ovarian cancer cells that can be therapeutically targeted. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - August 18, 2014 Category: Cancer & Oncology Source Type: research
GLUT3 is induced during epithelial-mesenchymal transition and promotes tumor cell proliferation in non-small cell lung cancer
Conclusions
Altogether, our results reveal that GLUT3 is a transcriptional target of ZEB1 and that this glucose transporter plays an important role in lung cancer, when tumor cells loose their epithelial characteristics to become more invasive. Moreover, these findings emphasize the development of GLUT3 inhibitory drugs as a targeted therapy for the treatment of patients with poorly differentiated tumors. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - July 29, 2014 Category: Cancer & Oncology Source Type: research
Defects in mitochondrial metabolism and cancer
Abstract
Cancer is a heterogeneous set of diseases characterized by different molecular and cellular features. Over the past decades, researchers have attempted to grasp the complexity of cancer by mapping the genetic aberrations associated with it. In these efforts, the contribution of mitochondria to the pathogenesis of cancer has tended to be neglected. However, more recently, a growing body of evidence suggests that mitochondria play a key role in cancer. In fact, dysfunctional mitochondria not only contribute to the metabolic reprogramming of cancer cells but they also modulate a plethora of cellul...
Source: Cancer and Metabolism - July 17, 2014 Category: Cancer & Oncology Source Type: research
Decoding the dynamics of cellular metabolism and the action of 3-bromopyruvate and 2-deoxyglucose using pulsed stable isotope-resolved metabolomics
Conclusions
By way of examples, we have applied this methodology to characterize central carbon metabolism of a panel of cancer cell lines and to determine the mode of metabolic inhibition of glycolytic inhibitors in times ranging from minutes to hours. Using pSIRM, we observed that 2-deoxyglucose is a metabolic inhibitor, but does not directly act on the glycolytic cascade. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - June 30, 2014 Category: Cancer & Oncology Source Type: research
