Corrigendum: Fatty Acid Metabolism-Related lncRNAs Are Potential Biomarkers for Predicting the Overall Survival of Patients With Colorectal Cancer

Red and processed meat have been associated with increased risk of colorectal cancer (CRC), whereas long-term use of non-steroid anti-inflammatory drugs (NSAIDs) may reduce the risk. The aim was to investigate potential interactions between meat intake, NSAID use, and gene variants in fatty acid metabolism and NSAID pathways in relation to the risk of CRC. A nested case-cohort study of 1038 CRC cases and 1857 randomly selected participants from the Danish prospective “Diet, Cancer and Health” study encompassing 57,053 persons was performed using the Cox proportional hazard models. Gene variants in SLC25A20, PRKAB1, LPCAT1, PLA2G4A, ALOX5, PTGER3, TP53, CCAT2, TCF7L2, BCL2 were investigated. CCAT2 rs6983267 was associated with risk of CRC per se (p<0.01). Statistically significant interactions were found between intake of red and processed meat and CCAT2 rs6983267, TP53 rs1042522, LPCAT1 rs7737692, SLC25A20 rs7623023 (pinteraction=0.04, 0.04, 0.02, 0.03, respectively), and use of NSAID and alcohol intake and TP53 rs1042522 (pinteraction=0.04, 0.04, respectively) in relation to risk of CRC. No other consistent associations or interactions were found. This study replicated an association of CCAT2 rs6983267 with CRC and an interaction between TP53 rs1042522 and NSAID in relation to CRC. Interactions between genetic variants in fatty acid metabolism and NSAID pathway and intake of red and processed meat were found. Our results suggest that meat intake and NSAID use affect the same carcinogenic mechanisms. All new findings should be sought replicated in independent prospective studies. Future studies on the cancer-protective effects of aspirin/NSAID should include gene and meat assessments.

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Polymorphisms in fatty acid metabolism-related genes are associated with colorectal cancer risk

Carcinogenesis ◽

10.1093/carcin/bgp325 ◽

2009 ◽

Vol 31 (3) ◽

pp. 466-472 ◽

Cited By ~ 45

Author(s):

Birgit Hoeft ◽

Jakob Linseisen ◽

Lars Beckmann ◽

Karin Müller-Decker ◽

Federico Canzian ◽

...

Keyword(s):

Colorectal Cancer ◽

Fatty Acid ◽

Cancer Risk ◽

Fatty Acid Metabolism ◽

Acid Metabolism ◽

Colorectal Cancer Risk

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SEMA3F-deficient colorectal cancer cells Promote lymphangiogenesis: fatty acid metabolism replace glycolysis for energy supply during lymphatic endothelial cells proliferation in tumor hypoxia microenvironment

10.1101/869644 ◽

2019 ◽

Author(s):

Xiaoyuan Fu ◽

Miaomiao Tao ◽

Hongbo Ma ◽

Cancan Wang ◽

Yanyan Li ◽

...

Keyword(s):

Colorectal Cancer ◽

Fatty Acids ◽

Endothelial Cells ◽

Fatty Acid ◽

Fatty Acid Metabolism ◽

Acid Metabolism ◽

Aerobic Glycolysis ◽

Peroxisome Proliferator ◽

Lymphatic Endothelial Cells ◽

Peroxisome Proliferator Activated Receptor

Abstractlymphangiogenesis as a process is colorectal cancer first metastasis via lymphatic vessels to proximal lymph nodes. The fuel metabolism in mitochondrial and support proliferation of lymphatic endothelial cells (LECs) remain elusive during lymphangiogenesis in tumor hypoxic microenvironment. Recent studies report that loss of SEMA3F critically contributes to lymphangiogenesis of the CRCs. Here, we silenced SEMA3F expression of CRCs and co-culture with hLECs, the tubulogenesis capacity and hLECs migration were escalated in the hypoxia, the hLECs mainly relied on fatty acid metabolism not aerobic glycolysis during lymphangiogenesis. SEMA3F-deficient CRCs up-regulated PMAKP expression and phosphorylation of hLECs, and activated its peroxisome proliferator-activated receptor (PPARs) and Peroxisome proliferator–activated receptor gamma coactivator-1 alpha (PGC-1a) facilitated their switched toward fatty acids (FA) catabolism. Furthermore, we observed that activation of the PGCI-PPAR lipid oxidation signaling pathway in hLECs was caused by the secretion of interleukin-6 by tumor cells.Taken together, this study indicates that CRCs with SEMA3F expression depletion significantly promotes lymphangiogenesis in hypoxia and faciliates the secretion of IL-6 in tumor cell, and activates mitochondria fatty acids oxidation (FAO) reaction in the hLECs by PGCI-PPAR signaling pathways to support its growth.

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Intake of Red and Processed Meat, Use of Non-Steroid Anti-Inflammatory Drugs, Genetic Variants and Risk of Colorectal Cancer: A Prospective Study of the Danish “Diet, Cancer and Health” Cohort

International Journal of Molecular Sciences ◽

10.3390/ijms20051121 ◽

2019 ◽

Vol 20 (5) ◽

pp. 1121 ◽

Cited By ~ 4

Author(s):

Vibeke Andersen ◽

Ulrich Halekoh ◽

Anne Tjønneland ◽

Ulla Vogel ◽

Tine Kopp

Keyword(s):

Colorectal Cancer ◽

Fatty Acid ◽

Fatty Acid Metabolism ◽

Genetic Variants ◽

Acid Metabolism ◽

Processed Meat ◽

Gene Variants ◽

Meat Intake ◽

Inflammatory Drugs ◽

Red And Processed Meat

Red and processed meat have been associated with increased risk of colorectal cancer (CRC), whereas long-term use of non-steroid anti-inflammatory drugs (NSAIDs) may reduce the risk. The aim was to investigate potential interactions between meat intake, NSAID use, and gene variants in fatty acid metabolism and NSAID pathways in relation to the risk of CRC. A nested case-cohort study of 1038 CRC cases and 1857 randomly selected participants from the Danish prospective “Diet, Cancer and Health” study encompassing 57,053 persons was performed using the Cox proportional hazard model. Gene variants in SLC25A20, PRKAB1, LPCAT1, PLA2G4A, ALOX5, PTGER3, TP53, CCAT2, TCF7L2, and BCL2 were investigated. CCAT2 rs6983267 was associated with the risk of CRC per se (p < 0.01). Statistically significant interactions were found between intake of red and processed meat and CCAT2 rs6983267, TP53 rs1042522, LPCAT1 rs7737692, SLC25A20 rs7623023 (pinteraction = 0.04, 0.04, 0.02, 0.03, respectively), and the use of NSAID and alcohol intake and TP53 rs1042522 (pinteraction = 0.04, 0.04, respectively) in relation to the risk of CRC. No other consistent associations or interactions were found. This study replicated an association of CCAT2 rs6983267 with CRC and an interaction between TP53 rs1042522 and NSAID in relation to CRC. Interactions between genetic variants in fatty acid metabolism and NSAID pathways and the intake of red and processed meat were found. Our results suggest that meat intake and NSAID use affect the same carcinogenic mechanisms. All new findings should be sought replicated in independent prospective studies. Future studies on the cancer-protective effects of aspirin/NSAID should include gene and meat assessments.

Download Full-text