Human mitochondrial MTHFD2 is a dual redox cofactor-specific methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase
ConclusionThese results show that the mitochondrial folate pathway isozymes MTHFD2 and MTHFD2L both exhibit dual redox cofactor specificity. Our kinetic analysis clearly supports a role for MTHFD2 in mitochondrial NADPH production, indicating that this enzyme is likely responsible for mitochondrial production of both NADH and NADPH in rapidly proliferating cells. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - December 6, 2017 Category: Cancer & Oncology Source Type: research
PKM2 is not required for colon cancer initiated by APC loss
ConclusionsPKM2 is not required forApc-deficient colon cancer or for nuclear translocation of β-catenin inApc-null tumor cells. These findings suggest that PKM2 expression is not required for colon tumor formation or progression. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - November 30, 2017 Category: Cancer & Oncology Source Type: research
Metabolomics guided pathway analysis reveals link between cancer metastasis, cholesterol sulfate, and phospholipids
ConclusionsUsing an integrated metabolomic workflow, this study identified a link between cholesterol sulfate and phospholipids, metabolic characteristics of the metastatic niche, and the capacity of tumor cells to colonize distant sites. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - October 31, 2017 Category: Cancer & Oncology Source Type: research
Molecular features that predict the response to antimetabolite chemotherapies
ConclusionsThis study demonstrates through unbiased analyses that the activities of metabolic pathways likely contribute to therapeutic response. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - October 3, 2017 Category: Cancer & Oncology Source Type: research
Bortezomib resistance in multiple myeloma is associated with increased serine synthesis
ConclusionsOur findings indicate that interfering with serine metabolism may be a novel strategy to improve bortezomib therapy and identify PHGDH as a potential biomarker for BTZ resistance. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - August 29, 2017 Category: Cancer & Oncology Source Type: research
Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities
ConclusionsSimilar to the genomic heterogeneity observed in TNBC, our results reveal metabolic heterogeneity among TNBC subtypes and demonstrate that understanding metabolic profiles and drug responses may prove valuable in targeting TNBC subtypes and identifying therapeutic susceptibilities in TNBC patients. Perturbation of metabolic pathways sensitizes TNBC to inhibition of receptor tyrosine kinases. Such metabolic vulnerabilities offer promise for effective therapeutic targeting for TNBC patients. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - August 22, 2017 Category: Cancer & Oncology Source Type: research
HIF prolyl hydroxylase PHD3 regulates translational machinery and glucose metabolism in clear cell renal cell carcinoma
ConclusionsOur findings suggest crucial involvement of PHD3 in the maintenance of key cellular functions including glycolysis and protein synthesis in ccRCC. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - July 4, 2017 Category: Cancer & Oncology Source Type: research
The action of β-hydroxybutyrate on the growth, metabolism and global histone H3 acetylation of spontaneous mouse mammary tumours: evidence of a β-hydroxybutyrate paradox
ConclusionsThese results suggest that a β-OHB paradox may occur in these mammary tumours in a manner analogous to the butyrate paradox. At low β-OHB concentrations (<1 mM, as observed in our tumour model post-treatment), and in the absence of a Warburg effect, β-OHB is consumed and thus acts as an oxidative energy source and not as an epigenetic factor. This would explain the increase in tumour growth after treatment, the metabolic profiles and the absence of a n effect on histone H3 acetylation. (Source: Cancer and Metabolism)
Source: Cancer and Metabolism - February 27, 2017 Category: Cancer & Oncology Source Type: research
