Interaction of Dietary Fatty Acids with Tumour Necrosis Factor Family Cytokines during Colon Inflammation and Cancer

Abstract

Intestinal homeostasis is precisely regulated by a number of endogenous regulatory molecules but significantly influenced by dietary compounds. Malfunction of this system may result in chronic inflammation and cancer. Dietary essential n-3 polyunsaturated fatty acids (PUFAs) and short-chain fatty acid butyrate produced from fibre display anti-inflammatory and anticancer activities. Both compounds were shown to modulate the production and activities of TNF family cytokines. Cytokines from the TNF family (TNF-α, TRAIL, and FasL) have potent inflammatory activities and can also regulate apoptosis, which plays an important role in cancer development. The results of our own research showed enhancement of apoptosis in colon cancer cells by a combination of either docosahexaenoic acid (DHA) or butyrate with TNF family cytokines, especially by promotion of the mitochondrial apoptotic pathway and modulation of NFκB activity. This review is focused mainly on the interaction of dietary PUFAs and butyrate with these cytokines during colon inflammation and cancer development. We summarised recent knowledge about the cellular and molecular mechanisms involved in such effects and outcomes for intestinal cell behaviour and pathologies. Finally, the possible application for the prevention and therapy of colon inflammation and cancer is also outlined.

Revisit dietary fiber on colorectal cancer: butyrate and its role on prevention and treatment

“…The relationship between inflammation and cancer promotion and progression has already been postulated [40], with evidences of the involvement of several pro-inflammatory cytokines [like tumor necrosis factor (TNF), interleukins (IL), chemokines], inflammation-inducing enzymes [like cyclooxygenase-2 (COX-2) and matrix metalloproteinase-9 (MMP-9)], adhesion molecules, and transcription factor activation [such as nuclear factor κB (NF-κB) and hypoxiainducing factor 1α (HIF-1α)] that results in inflammatory gene products [16,23]. These gene products, essentially controlled by NF-κB, are strictly linked with the carcinogenic process, since they are related with tumor cell survival, antiapoptotic signaling pathways, proliferation, invasion, and angiogenesis [16].…”

“…Chronic intestinal inflammation that characterizes patients with inflammatory bowel disease (IBD), namely Crohn's disease and ulcerative colitis, may be related with colorectal cancer pathogenesis [40]. Butyrate-producing bacteria as well as butyrate concentration in fecal samples were found decreased in patients with ulcerative colitis in comparison with healthy individuals.…”

Dietary Fiber Intake Modifies the Positive Association between n–3 PUFA Intake and Colorectal Cancer Risk in a Caucasian Population

“…The possible interaction between dietary FA and DF intakes has been previously shown in a population-based case-control study (17). Also, recently, an interaction has been reported of dietary n-3 PUFA and shortchain FA intakes produced from fiber with cytokines during colon inflammation and cancer (55). In addition, the studies reporting a positive association between n-3 PUFA intake and advanced CRC or CRC included subjects with low consumption of DF intake (median: 10-14 g/d; mean: 17-19 g/d) (36,39), whereas the studies reporting no association between n-3 PUFA intake and CRC included subjects with a higher median DF intake (16-23 g/d) (40).…”

OCT4B1 promotes cell growth, migration and invasion suppressing sensitivity to οxaliplatin in colon cancer

“…Alteration of oncogenes or tumor-suppressor activity often occurs at the critical points of the development of colon cancer (4). For example, cytokines from the TNF family have potent inflammatory activities and play an important role in cancer development by regulating apoptosis in colon cancer (5). Chen et al reported that the tumor suppressor p53 promotes mitochondrial DNA base excision to regulate the development of colon cancer (6).…”