Tuesday, August 9, 2016

Scientists reveal how tumor cells exploit function of mitochondria to support the proliferation of cancer

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Scientists reveal how tumor cells exploit function of mitochondria to support the proliferation of cancer -

As the central cells, mitochondria are critical for every organization because of their role in energy production while also monitoring the survival, but the way they work in cancer is not fully known. This is particularly important because, in general, tumor cells proliferate more than normal tissue, and scientists have speculated that the mechanisms that maintain mitochondrial function are responsible for supporting the expansion of the tumor.
Now Wistar Institute's scientists have identified a specific network of proteins in the mitochondria of tumor cells which is essential for the maintenance of mitochondrial cleaning function, which not only allows the proliferation of tumor cells, but also their ability to move and invade distant organs. By understanding the actors involved, the Wistar scientists have been able to disable individual subunits within the network, greatly reducing the ability of cancer cells to grow and spread, suggesting an attractive new therapeutic target. The results were published in the journal PLoS Biology.
"This is an example of how tumors can quickly adapt to meet their own needs biosynthetic higher," said Dario C. Altieri, MD, president and CEO of the Wistar Institute, Director the Wistar Institute cancer Centre, Robert & Penny Fox distinguished Professor and lead author of the study. "mitochondria play a crucial role in the ability of a tumor to treat the energy to grow and spread to to identify the mechanisms of how tumors maintain mitochondrial function and operate to support the abnormal cell proliferation and metastasis can discover new therapeutic targets in a wide variety of cancers. "
previous studies have provided evidence that the ability to control the folding and stability of proteins, or proteostasis, the importance of reducing cellular stress. It has also been known that tumors hijack proteostasis mechanisms to their advantage, but how this happened in the mitochondria remained largely unknown. The network described by the Wistar scientists answered this question and confirmed its important role in tumor development. In particular, one of the components of this network - ClpP - was found universally overexpressed in primary human cancer and metastatic and is correlated with shortened survival of patients. In this single study, the scientists identified the overexpression of this subunit in breast, prostate, colon and lung, as well as melanoma and lymphoma.
"There is little interest in targeting pathways involved in mitochondrial function, and we have identified such a way that can provide a target" drugable "for a variety of cancers," said Seo Jae Ho, Ph.D., a postdoctoral fellow in the laboratory at Wistar Altieri and first author of the study. "Other studies have shown that it is possible to target mitochondrial proteins in preclinical models to disrupt the network, we identified in this study could stop key processes that lead to the progression of the tumor."


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