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Title:
Colorectal Cancer and Metabolism | Current Colorectal Cancer Reports
Description:
Purpose of Review Metabolic reprogramming is essential for the rapid proliferation of cancer cells and is thus recognized as a hallmark of cancer. In this review, we will discuss the etiologies and effects of metabolic reprogramming in colorectal cancer. Recent Findings Changes in cellular metabolism may precede the acquisition of driver mutations ultimately leading to colonocyte transformation. Oncogenic mutations and loss of tumor suppressor genes further reprogram CRC cells to upregulate glycolysis, glutaminolysis, one-carbon metabolism, and fatty acid synthesis. These metabolic changes are not uniform throughout tumors, as subpopulations of tumor cells may rely on different pathways to adapt to nutrient availability in the local tumor microenvironment. Finally, metabolic cross-communication between stromal cells, immune cells, and the gut microbiota enable CRC growth, invasion, and metastasis. Summary Altered cellular metabolism occurs in CRC at multiple levels, including in the cells that make up the bulk of CRC tumors, cancer stem cells, the tumor microenvironment, and host-microbiome interactions. This knowledge may inform the development of improved screening and therapeutics for CRC.
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Keywords {๐}
pubmed, cancer, google, scholar, article, cas, colorectal, central, cell, metabolism, metabolic, cells, colon, stem, wang, tumor, res, biol, mol, reprogramming, expression, sci, human, review, science, gut, growth, med, glucose, lipid, nature, genes, crc, rep, signaling, mutations, fatty, acid, oncol, gene, intestinal, mitochondrial, williams, cellular, molecular, warburg, oncotarget, zhang, role, patients,
Topics {โ๏ธ}
month download article/chapter patient-derived xenograft model akt phosphorylates hk-ii mediate r-spondin signalling stem cell epigenetics low-density lipoprotein receptor local tumor microenvironment specific butyrate-producing bacteria short-chain fructo-oligosaccharides selectively kills kras akt-directed glucose metabolism butyrate-mediated histone acetylation hr-mas nmr spectroscopy wnt/ฮฒ-catenin signaling reactive oxygen species hif-2ฮฑ target genes crypt stem cells full article pdf lipid metabolism-related genes biochim biophys acta butyrate-mediated growth inhibition wild-type p53 fatty acid synthase include metabolic reprogramming glucose metabolism research mitochondrial pyruvate metabolism colorectal cancerโmolecular pathogenesis lgr5 homologues associate measure energy metabolism mitochondrial pyruvate carrier mitochondrial dna depletion fatty acid synthesis privacy choices/manage cookies glycolytic enzymes mediated marker gene lgr5 intestinal stem cells targeting warburg effect biochem soc trans pyruvate dehydrogenase kinase schell jc fatty acid composition intestinal stem cell p53 target gene van vranken jg promote tumor growth reverse warburg effect warburg effect dictates sorted stem cells tumour microenvironment dilemma butyrate-producing bacteria
Questions {โ}
- Cellular metabolism and disease: what do metabolic outliers teach us?
- Field cancerisation in colorectal cancer: a new frontier or pastures past?
- Field cancerization in the colon: a role for aberrant DNA methylation?
- Friend or foe?
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headline:Colorectal Cancer and Metabolism
description:Metabolic reprogramming is essential for the rapid proliferation of cancer cells and is thus recognized as a hallmark of cancer. In this review, we will discuss the etiologies and effects of metabolic reprogramming in colorectal cancer. Changes in cellular metabolism may precede the acquisition of driver mutations ultimately leading to colonocyte transformation. Oncogenic mutations and loss of tumor suppressor genes further reprogram CRC cells to upregulate glycolysis, glutaminolysis, one-carbon metabolism, and fatty acid synthesis. These metabolic changes are not uniform throughout tumors, as subpopulations of tumor cells may rely on different pathways to adapt to nutrient availability in the local tumor microenvironment. Finally, metabolic cross-communication between stromal cells, immune cells, and the gut microbiota enable CRC growth, invasion, and metastasis. Altered cellular metabolism occurs in CRC at multiple levels, including in the cells that make up the bulk of CRC tumors, cancer stem cells, the tumor microenvironment, and host-microbiome interactions. This knowledge may inform the development of improved screening and therapeutics for CRC.
datePublished:2018-11-16T00:00:00Z
dateModified:2018-11-16T00:00:00Z
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Metabolism
Colorectal cancer
Warburg effect
Cancer stem cells
Tumor microenvironment
Microbiome
Oncology
Proctology
Colorectal Surgery
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headline:Colorectal Cancer and Metabolism
description:Metabolic reprogramming is essential for the rapid proliferation of cancer cells and is thus recognized as a hallmark of cancer. In this review, we will discuss the etiologies and effects of metabolic reprogramming in colorectal cancer. Changes in cellular metabolism may precede the acquisition of driver mutations ultimately leading to colonocyte transformation. Oncogenic mutations and loss of tumor suppressor genes further reprogram CRC cells to upregulate glycolysis, glutaminolysis, one-carbon metabolism, and fatty acid synthesis. These metabolic changes are not uniform throughout tumors, as subpopulations of tumor cells may rely on different pathways to adapt to nutrient availability in the local tumor microenvironment. Finally, metabolic cross-communication between stromal cells, immune cells, and the gut microbiota enable CRC growth, invasion, and metastasis. Altered cellular metabolism occurs in CRC at multiple levels, including in the cells that make up the bulk of CRC tumors, cancer stem cells, the tumor microenvironment, and host-microbiome interactions. This knowledge may inform the development of improved screening and therapeutics for CRC.
datePublished:2018-11-16T00:00:00Z
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Metabolism
Colorectal cancer
Warburg effect
Cancer stem cells
Tumor microenvironment
Microbiome
Oncology
Proctology
Colorectal Surgery
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