{"id":72409,"date":"2022-03-22T11:45:51","date_gmt":"2022-03-22T10:45:51","guid":{"rendered":"https:\/\/www.pcb.ub.edu\/connection-shown-between-glucose-metabolism-and-colorectal-tumorigenesis\/"},"modified":"2022-03-24T17:14:01","modified_gmt":"2022-03-24T16:14:01","slug":"connection-shown-between-glucose-metabolism-and-colorectal-tumorigenesis","status":"publish","type":"post","link":"https:\/\/www.pcb.ub.edu\/en\/connection-shown-between-glucose-metabolism-and-colorectal-tumorigenesis\/","title":{"rendered":"Connection shown between glucose metabolism and colorectal tumorigenesis"},"content":{"rendered":"

An international team of researchers, led by Dr Carlos Sebasti\u00e1n Mu\u00f1oz, a Beatriz Galindo researcher and director of the UB Metabolic Dynamics in Cancer Laboratory<\/a> at the Barcelona Science Park, has identified a type of cells in the intestines, characterised by their high glucose metabolism, that behave like stem cells and could be responsible for the genesis and spread of colorectal cancer. The results of the study, published in Nature Communications<\/a>, open up a new path for research to design new, more effective therapeutic targets for this type of tumour, based on blocking the metabolic reprogramming of these cells.<\/strong><\/p>\n

The study was led jointly by Dr Carlos Sebasti\u00e1n<\/strong>\u00a0and Prof Raul Mostoslavsky <\/strong>from the Massachusetts General Hospital Cancer Center<\/a> (associated with Harvard Medical School<\/a>), with participation from renowned researchers at the Candiolo Cancer Institute-FPO<\/a> (Turin, Italy) and several hospitals and departments of Harvard University.<\/p>\n

Colorectal cancer is one of the most common types of cancer in Spain, in both women and men, with 40,000 cases diagnosed in 2021 according to the Asociaci\u00f3n Espa\u00f1ola Contra el C\u00e1ncer (AECC). Despite recent advances in diagnosis and treatment of this type of cancer, its mortality rate remains very high: the second most common cause of cancer-related deaths. So, it is important to get a better understanding of the mechanisms involved in the genesis and spread of these tumours.<\/p>\n

Role of glucose metabolism in intestinal tumours<\/strong><\/h3>\n

Cancerous cells don\u2019t metabolise glucose in the same way as normal cells. \u201cIn previous studies, we showed that glucose metabolism plays a key role in the initiation of intestinal tumours in murine models of colorectal cancer. Now, in this study, we\u2019ve discovered a rare population of cells in \u00a0these tumours characterised by their high rates of glucose metabolism (glycolytic cells) and that behave like stem cells, meaning they are pluripotent and can initiate a tumour,\u201d explains Dr Carlos Sebasti\u00e1n<\/strong>, member of the Department of Cell Biology, Physiology and Immunology<\/a> in the Faculty of Biology at the University of Barcelona (UB) and the Institute of Biomedicine of the University of Barcelona (IBUB<\/a>).<\/p>\n

The results show that intestinal tumours are metabolically heterogeneous and suggest that there is a hierarchy in which a small population of highly glycolytic cells are responsible for tumour initiation and spread.<\/p>\n

\u201cTo analyse this heterogeneity, we developed a novel system that, in combination with intestinal organoids (3D cultures that imitate the cell composition of the intestine), has allowed us to visualise, track and characterise cells with different metabolic properties in the intestinal epithelium and in tumours at the single-cell level. The characterisation of these glycolytic cells has led us to discover that they act as intestinal stem cells and that this cell type is also found in intestinal tumours,\u201d explains Dr Sebasti\u00e1n<\/strong>.<\/p>\n

\"\"

Immunofluorescence image showing cells with different metabolic properties within the intestinal epithelium (Author: Carlos Sebasti\u00e1n).<\/p><\/div>\n

\u00a0<\/strong>Metabolic reprogramming in the tumour process<\/strong><\/h3>\n

One of the main characteristics of tumour cells is their ability to change their metabolism (metabolic reprogramming) to grow, survive and proliferate, which is intimately linked to tumour progression, metastasis and therapeutic resistance.<\/p>\n

Traditionally, the scientific community has considered these metabolic alterations mere adaptations geared towards providing the energy and macromolecules needed for cell proliferation. \u201cHowever, our studies show that this metabolic reprogramming occurs at very early stages during tumorigenesis and is intrinsically associated to cell fate determination,\u201d reveals the scientist.<\/p>\n

Plus, the team of researchers has discovered that blocking metabolic reprogramming is enough to inhibit the glycolytic cells\u2019 ability to form intestinal tumours. \u201cGiven that these tumour-initiating cells are involved in tumour progression, metastasis and relapse, our results suggest that this metabolic vulnerability could be used to treat colorectal cancer,\u201d he adds.<\/p>\n

Another important conclusion from the study is that these glycolytic cells are quiescent, meaning they don\u2019t proliferate, which challenge the dogma that this metabolic reprogramming is associated with biomass production and cell proliferation. In fact, the researchers observed that these metabolic characteristics are necessary to protect these cells from oxidative stress and maintain their stem cell potential.<\/p>\n

\u201cAlthough these studies were conducted with mouse models of colon cancer and, therefore, we must be prudent in transferring them to the human disease, the results obtained could be useful in the future for designing new, more effective therapies for this type of cancer. In this regard, our laboratory continues working in this line with samples from colon cancer patients to apply our findings to these patients,\u201d the researcher highlights.<\/p>\n

\u00bb Reference article:<\/strong> Sebasti\u00e1n C*, Ferrer C, Serra M, Choi JE, Ducano N, Mira A, Shah MS, Stopka SA, Perciaccante AJ, Isella C, Moya-Rull D, Vara-Messler M, Giordano S, Maldi E, Desay N, Capen DE, Medico E, Cetinbas M, Sadreyev RI, Brown D, Rivera MN, Sapino A, Breault DT, Agar NYR, Mostoslavsky R*. \u201c A non-dividing cell population with high pyruvate dehydrogenase kinase activity regulates metabolic heterogeneity and tumorigenesis in the intestine\u201d<\/em>. Nature Communications (2022). DOI: https:\/\/doi.org\/10.1038\/s41467-022-29085-y<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

An international team of researchers, led by Dr Carlos Sebasti\u00e1n Mu\u00f1oz, a Beatriz Galindo researcher and director of the UB Metabolic Dynamics in Cancer Laboratory at the Barcelona Science Park,…<\/p>\n","protected":false},"author":14,"featured_media":72313,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":""},"categories":[36],"tags":[],"class_list":["post-72409","post","type-post","status-publish","format-standard","has-post-thumbnail","category-science"],"acf":[],"yoast_head":"\nConnection shown between glucose metabolism and colorectal tumorigenesis - Parc Cient\u00edfic de Barcelona<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.pcb.ub.edu\/en\/connection-shown-between-glucose-metabolism-and-colorectal-tumorigenesis\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Connection shown between glucose metabolism and colorectal tumorigenesis - 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