<p>Publication in Nature: researchers from the Université Libre de Bruxelles (ULB) discovered the key role of the extracellular environment in dictating the ability of mutated cells to induce cancer formation. </p>
Reactive compounds cause cellular damage that is suspected to contribute to aging and neurodegenerative diseases. Oxidative stress and environmental factors likely contribute to this. Here we report that an enzyme mutated in Parkinson’s disease can prevent damage of metabolites and proteins caused by a metabolite from the central pathway of sugar metabolism. Inactivation of this enzyme in model systems, ranging from flies to human cells, leads to the accumulation of a wide range of damaged metabolites and proteins. Thus, this enzyme represents a highly conserved strategy to prevent damage in cells that metabolize sugars. Overall, we discovered a fundamental link between carbohydrate metabolism and a type of cellular damage that might contribute to the development of Parkinson’s disease.
Mass spectrometry proteomics data have been deposited at ProteomeXchange, [www.proteomexchange.org/][1] (accession no. PXD029410) via the PRIDE partner repository ([62][2]). Processed mass spectrom
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Metaplasia is defined as the replacement of a fully differentiated cell type by another. There are several classical examples of metaplasia, one of the most frequent is called Barrett s oesophagus. Barrett s oesophagus is characterized by the replacement of the keratinocytes by columnar cells in the lower oesophagus upon chronic acid reflux. This metaplasia is considered a precancerous lesion that increases by around 50 times the risk of this oesophageal adenocarcinoma. Nonetheless, the mechanisms involved in the development of metaplasia in the oesophagus are still partially unknown.
In a new study published in
Cell Stem Cell, researchers led by Mr. Benjamin Beck, (FNRS research associate and WELBIO investigator at the IRIBHM, Université libre de Bruxelles, Belgium), report the mechanisms involved in the transdifferentiation of oesophageal keratinocytes into columnar cells.
Cancer: Tumor driver promoting EMT, metastasis and resistance to therapy
Cancer metastasis, which is the dissemination of tumor cells into distant organs, is the leading cause of mortality in cancer patients. To undergo metastasis, cells must leave the primary tumor, circulate into the blood, colonize distant organs, and form distant metastasis. It has been proposed that epithelial to mesenchymal transition (EMT), a process in which epithelial cells detach from their neighboring cells, and acquire mesenchymal migrating properties, is important to initiate the metastatic cascade allowing the cancer cells to leave the primary tumor. However, the role of genetic mutations in promoting EMT is unknown.