NFκB: a promising target for natural products in cancer chemoprevention

Luqman, Suaib; Pezzuto, John M.

doi:10.1002/ptr.3171

Cited by 179 publications

(125 citation statements)

References 194 publications

(138 reference statements)

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“…NF-κB can modulate the transcriptional activation of genes associated with cell proliferation, angiogenesis, metastasis, tumor promotion and suppression of apoptosis (Lugman and Pezzuto, 2010). Researches have shown that disregulation of NF-κB transcription machinery is one of the factors thought to be common early events in malignant tumor progression (Meng et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Tao¹,

Zhang²,

Ma³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Triptolide, a diterpenoid obtained from Tripteryglum wilfordii Hook.f, has attracted interest for its antitumor activities against human tumor cell lines in recent years. This report focuses on anti-proliferative and pro-apoptotic activities in human melanoma A375 cells assessed by CCK8 assay, Hoechst 33258 staining and flow cytometry. In addition, triptolide-induced arrest in the S phase was also observed. Caspase assays showed the apoptosis induced by triptolide was caspase-dependent and probably through intrinsic apoptotic pathways. Furthermore, expression of NF-kB (p65) and its downstream factors such as Bcl-2, Bcl-X L was down-regulated. Taken together, the data indicate that triptolide inhibits A375 cells proliferation and induces apoptosis by a caspase-dependent pathway and through a NF-kB-mediated mechanism.

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Section: Discussionmentioning

confidence: 99%

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Tao¹,

Zhang²,

Ma³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…As a result of its key role in several pathologic conditions, NF-κB is a major drug target in a variety of diseases. The blockade of NF-κB transcriptional activity in microglial is also known to suppress expression of iNOS, COX-2, pro-inflammatory cytokines and chemokines including TNF-α, IL-1β and MCP-1 (38)(39)(40). Therefore, many putative anti-inflammatory therapies seek to block NF-κB activity.…”

Section: Discussionmentioning

confidence: 99%

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

Choi¹

2012

Int J Mol Med

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Abstract. Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, has been reported to exhibit anti-inflammatory and antitumor activities. However, the cellular and molecular mechanisms underlying the naringenin anti-inflammatory activity are poorly understood. In this study, we conducted an investigation of the inhibitory effects of naringenin on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators in BV2 microglial cells. We found that pre-treatment with naringenin prior to treatment with LPS significantly inhibited excessive production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) in a dose-dependent manner. The inhibition was associated with downregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Naringenin also attenuated the production of pro-inflammatory cytokines and chemokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) by suppressing expression of mRNAs for these proteins. In addition, the molecular mechanism underlying naringenin-mediated attenuation in BV2 cells has a close relationship to suppressing translocation of the nuclear factor-κB (NF-κB) p65 subunit into the nucleus and the phosphorylation of Akt and mitogen-activated protein kinases (MAPKs). These findings suggest that naringenin may provide neuroprotection through suppression of pro-inflammatory pathways in activated BV2 microglial cells.

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“…The blockade of NF-κB transcriptional activity is also known to suppress expression of pro-inflammatory mediators including iNOS, COX-2, and IL-1β (37)(38)(39). Therefore, downregulation of NF-κB activity is a useful strategy to regulate inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

7,8-Dihydroxyflavone exhibits anti-inflammatory properties by downregulating the NF-κB and MAPK signaling pathways in lipopolysaccharide-treated RAW264.7 cells

et al. 2012

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Abstract. 7,, a member of the flavonoid family, has received considerable attention as a selective tyrosine kinase receptor B agonist. Several studies have indicated that 7,8-DHF has neurotrophic and antioxidant activities. However, little is known about the cellular and molecular mechanisms underlying the anti-inflammatory activity of 7,8-DHF. Therefore, we investigated whether 7,8-DHF affects the expression of inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Our results indicated that 7,8-DHF significantly attenuated secretion of LPS-induced inflammatory mediators nitric oxide (NO), prostaglandin E 2 (PGE 2 ) and interleukin-1β (IL-1β) in RAW264.7 cells. Additionally, LPS-induced expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2 and IL-1β was decreased by pre-treatment with 7,8-DHF. Our results also showed that 7,8-DHF reduces LPS-induced nuclear factor-κB (NF-κB) activity via the suppression of the nuclear translocation of NF-κB p65 and the degradation of inhibitor κB (lκB). In addition, 7,8-DHF inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) such as extracellular-signal-related kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). These results suggest that the anti-inflammatory property of 7,8-DHF is related to the downregulation of iNOS, COX-2 and IL-1β, due to NF-κB inhibition as well as to the negative regulation of MAPK activation in RAW264.7 cells. Thus, 7,8-DHF may be a novel therapeutic agent for the prevention of various inflammatory diseases.

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NFκB: a promising target for natural products in cancer chemoprevention

Cited by 179 publications

References 194 publications

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Triptolide Inhibits Proliferation and Induces Apoptosis of Human Melanoma A375 Cells

Naringenin attenuates the release of pro-inflammatory mediators from lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-κB and inhibiting mitogen-activated protein kinases

7,8-Dihydroxyflavone exhibits anti-inflammatory properties by downregulating the NF-κB and MAPK signaling pathways in lipopolysaccharide-treated RAW264.7 cells

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