Effect of Curcumin on Nuclear Factor κB Signaling Pathways in Human Chronic Myelogenous K562 Leukemia Cells

Reuter, Simone; Charlet, Jessica; Juncker, Tom; Teiten, Marie-Hélène; Dicato, Mario; Diederich, Marc

doi:10.1111/j.1749-6632.2009.04731.x

Cited by 76 publications

(54 citation statements)

References 41 publications

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“…In order to answer that question, we decided to examine NF-κB. NF-κB is a central regulator of inflammatory cytokine secretion [52, 53]. Previous studies have shown that it is a key transcriptional regulator of IL6, IL8, and CCL5 cytokines.…”

Section: Resultsmentioning

confidence: 99%

Key roles of necroptotic factors in promoting tumor growth

et al. 2016

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Necroptotic factors are generally assumed to play a positive role in tumor therapy by eliminating damaged tumor cells. Here we show that, contrary to expectation, necroptotic factors RIPK1, RIPK3, and MLKL promote tumor growth. We demonstrate that genetic knockout of necroptotic genes RIPK1, RIPK3, or MLKL in cancer cells significantly attenuated their abilities to grow in an anchorage-independent manner. In addition, they exhibited significantly enhanced radiosensitivity. The knockout cells also showed greatly reduced ability to form tumors in mice. Moreover, necrosulfonamide (NSA), a previously identified chemical inhibitor of necroptosis, could significantly delay tumor growth in a xenograft model. Mechanistically, we show that necroptoic factors play a significant role in maintaining the activity of NF-κB. Finally, we found that high levels of phosphorylated MLKL in human esophageal and colon cancers are associated with poor overall survival. Taken together, we conclude that pro-necroptic factors such as RIPK1, RIPK3, and MLKL may play a role in supporting tumor growth, and MLKL may be a promising target for cancer treatment.

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Section: Resultsmentioning

confidence: 99%

Key roles of necroptotic factors in promoting tumor growth

et al. 2016

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“…• Down-regulated the expression of 29 out of 84 TNF-a-activated NF-kB-associated genes in leukaemia cells (Reuter et al, 2009). …”

Section: Action Of Tnf-amentioning

confidence: 99%

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

338

239

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TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-a, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-a antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-a action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution. LINKED ARTICLESThis article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx

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“…Curcumin, a well-known epigenetic modifier [90–95], with anti-oxidant [96], anti-inflammatory [97], anti-proliferative [98], and anti-angiogenic [99] properties, has also been shown to have synergetic anti-cancer effects when combined with fish oil. For example, we have reported that the combination of fish oil and curcumin can antagonize NFκB activation in the mouse colon following the induction of chronic inflammation [100].…”

Section: Epigenetic Effects Of N–3 Pufamentioning

confidence: 99%

Mechanisms by Which Pleiotropic Amphiphilic n−3 PUFA Reduce Colon Cancer Risk

Chapkin

DeClercq

Kim

et al. 2014

Curr Colorectal Cancer Rep

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Colorectal cancer is one of the major causes of cancer-related mortality in both men and women worldwide. Genetic susceptibility and diet are primary determinants of cancer risk and tumor behavior. Experimental, epidemiological, and clinical data substantiate the beneficial role of n–3 polyunsaturated fatty acids (PUFA) in preventing chronic inflammation and colon cancer. From a mechanistic perspective, n–3 PUFA are pleiotropic and multifaceted with respect to their molecular mechanisms of action. For example, this class of dietary lipid uniquely alters membrane structure/ cytoskeletal function, impacting membrane receptor function and downstream signaling cascades, including gene expression profiles and cell phenotype. In addition, n–3 PUFA can synergize with other potential anti-tumor agents, such as fermentable fiber and curcumin. With the rising prevalence of diet-induced obesity, there is also an urgent need to elucidate the link between chronic inflammation in adipose tissue and colon cancer risk in obesity. In this review, we will summarize recent developments linking n–3 PUFA intake, membrane alterations, epigenetic modulation, and effects on obesity-associated colon cancer risk.

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Effect of Curcumin on Nuclear Factor κB Signaling Pathways in Human Chronic Myelogenous K562 Leukemia Cells

Cited by 76 publications

References 41 publications

Key roles of necroptotic factors in promoting tumor growth

Key roles of necroptotic factors in promoting tumor growth

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Mechanisms by Which Pleiotropic Amphiphilic n−3 PUFA Reduce Colon Cancer Risk

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