NF‐κB Signaling in Gastric Cancer

Sokolova, Olga; Naumann, Michael

doi:10.3390/toxins9040119

Cited by 176 publications

(129 citation statements)

References 188 publications

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“…The NF-κB signaling pathway is closely linked to the inflammatory state of the stomach [24]. Modulation of the NF-κB signaling is considered to be a therapeutic target in stomach diseases [25], and fermented lotus root may provide a novel therapeutic candidate.…”

Section: Discussionmentioning

confidence: 99%

Gastroprotective Effects of Fermented Lotus Root against Ethanol/HCl-Induced Gastric Mucosal Acute Toxicity in Rats

et al. 2020

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Gastric ulcers are a common gastrointestinal disease across the globe. Alcohol consumption is the primary cause of gastric carcinogenesis and progression. We investigated the gastroprotective effects of fermented lotus root (FL) against ethanol (EtOH)/HCl-induced gastric ulcers in a rat model and the conceivable underlying mechanisms involved. Rats received different doses of FL (50, 100, and 200 mg/kg) or ranitidine (positive control, 30 mg/kg) via oral gavage daily for 14 days. One hour after the last oral administration of FL, the EtOH/HCl mixture was orally intubated to induce gastric damage. Oral administration of FL significantly alleviated the gastric lesions. Moreover, FL also elevated the amounts of nitric oxide and the antioxidant enzyme activities of superoxide dismutase, glutathione peroxidase, and catalase in the stomach. To verify the gastric mucosal defense mechanism, inflammation-related genes were measured. Our results revealed that FL effectively inhibited gastric mucosal damage via downregulation of the nuclear factor-kappaB (NF-κB) response in the stomach. The administration of FL significantly lowered the gastric mRNA expression of inflammation-related genes, including NF-κb1, tumor necrosis factor-α, interferon γ, and prostaglandin-endoperoxide synthase 2, compared with the gastric ulcer control group. In addition, the NF-κB signaling pathway-related protein markers inhibitor of κB (IκB)-α, IκB kinase, and NF-κB were significantly reduced in the FL groups. Taken together, these data suggest that FL administration may have potential as an alternative treatment for gastric ulcers due to its antioxidant and anti-inflammatory effects and its ability to promote the recovery of gastric mucosa.

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Section: Discussionmentioning

confidence: 99%

Gastroprotective Effects of Fermented Lotus Root against Ethanol/HCl-Induced Gastric Mucosal Acute Toxicity in Rats

et al. 2020

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“…In addition, IKKα in macrophages has been shown to deliberately accelerate the promotion of c‐Rel and p65 yields and their removal from promoters of proinflammatory genes. Alkylation and oxidation of a redox‐sensitive cysteine, found at the DNA binding loop, also inhibits NF‐κβ proteins (Sokolova and Naumann ).…”

Section: Nf‐κβ Signaling At a Glancementioning

confidence: 99%

Nuclear factor‐kappa β as a therapeutic target for Alzheimer's disease

Jha¹,

Jha

Kar

et al. 2019

Journal of Neurochemistry

115

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Alzheimer's disease (AD) is a typical progressive, chronic neurodegenerative disorder with worldwide prevalence. Its clinical manifestation involves the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs). NFTs occur in brain tissues as a result of both Ab agglomeration and Tau phosphorylation. Although there is no known cure for AD, research into possible cures and treatment options continues using cell-cultures and model animals/organisms. The nuclear factor-kappa b (NF-jb) plays an active role in the progression of AD. Impairment to this signaling module triggers undesirable phenotypic changes such as neuroinflammation, activation of microglia, oxidative stress related complications, and apoptotic cell death. These imbalances further lead to homeostatic abnormalities in the brain or in initial stages of AD essentially pushing normal neurons toward the degeneration process. Interestingly, the role of NF-jb signaling associated receptor-interacting protein kinase is currently observed in apoptotic and necrotic cell death, and has been reported in brains. Conversely, the NF-jb signaling pathway has also been reported to be involved in normal brain functioning. This pathway plays a crucial role in maintaining synaptic plasticity and balancing between learning and memory. Since any impairment in the pathways associated with NF-jb signaling causes altered neuronal dynamics, neurotherapeutics using compounds including, antioxidants, bioflavonoids, and non-steroidal anti-inflammatory drugs against such abnormalities offer possibilities to rectify aberrant excitatory neuronal activity in AD. In this review, we have provided an extensive overview of the crucial role of NF-jb signaling in normal brain homeostasis. We have also thoroughly outlined several established pathomechanisms associated with NF-jb pathways in AD, along with their respective therapeutic approaches.

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“…Aberrant activation of NF-κB signaling is known to be critical for GC survival. 18,23,24 To verify whether LINC00365 is involved in NF-κB pathway regulation, we examined the phosphorylation of IκB by Western blotting and found that up-regulation of LINC00365 was accompanied by a decrease in IκB phosphorylation ( Figure 4A and B). Immunofluorescence revealed that LINC00365 overexpression inhibited translocation of the p65 subunit of NF-κB from the cytoplasm to the nucleus in GC cells ( Figure 4C).…”

Section: Linc00365 Inhibits Activation Of the Nf-κb Signaling Pathwaymentioning

confidence: 99%

“…16 Activated NF-κB triggers a series of molecular reactions, including the upregulation of protein-encoding genes involved in cell proliferation. 17,18 Claerhout et al found that the histone deacetylase inhibitor vorinostat up-regulated SCGB2A1 mRNA expression in GC cell lines AGS and KATO-III while inhibiting cell proliferation, suggesting that SCGB2A1 may be involved in the regulation of prosurvival signals in GC. 19 lncRNA may function through regulating the expression of encoding genes and this "lncRNA-encoding proteins pattern" has been demonstrated in a variety of tumors including GC.…”

Section: Introductionmentioning

confidence: 99%

<p>The LINC00365/SCGB2A1 (Mammaglobin B) Axis Down-Regulates NF-κB Signaling and Is Associated with the Progression of Gastric Cancer</p>

Yan

Zhang

Zhong

et al. 2020

CMAR

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A lack of early diagnostic biomarkers and therapeutic targets has led to poor prognosis for gastric cancer patients. However, the analysis of cancer-associated genomic data has been shown to be effective in identifying potential markers. Recently, the long noncoding RNA LINC00365 and SCGB2A1 gene (as known as mammaglobin B) were predicted to be co-expressed in gastric cancer based on the Gene Expression Omnibus database. However, their precise role in gastric cancer tumors is still not clear. Methods: The expressions of LINC00365 and SCGB2A1 in gastric cancer tissues were investigated using qPCR and their expressions were detected in a gastric cancer tissue microarray by in situ hybridization and immunohistochemical staining. The functions of LINC00365 in BGC-823 and MGC-803 gastric cancer cells were tested using the MTT assay, flow cytometry, colony formation assay, EDU staining, immunofluorescence and luciferase assay. Results: We found that LINC00365 and SCGB2A1 mRNA were both expressed at low levels in 30 cases of gastric cancer. Gastric cancer tissue microarray analysis indicated that LINC00365 and SCGB2A1 were expressed at low levels in tumor tissue, and low expression of both factors correlated with shorter survival time. Functional studies showed that LINC00365 overexpression significantly inhibited gastric cancer cell viability through the impairment of proliferation rather than the promotion of apoptosis. Furthermore, overexpressed LINC00365 upregulated SCGB2A1 in gastric cancer cell lines. Immuno-fluorescence and luciferase assay analysis indicated that LINC00365 overexpression inhibited the NF-κB prosurvival signaling pathway. Consistent with the effects of LINC00365, SCGB2A1 upregulation also reduced cell survival and inactivated NF-κB. Conclusion: Collectively, our findings revealed that SCGB2A1 may be the target coding protein regulated by LINC00365 in gastric cancer. LINC00365 and SCGB2A1 may function as tumor suppressors and may serve as potential prognostic and therapeutic markers in gastric cancer treatment.

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NF‐κB Signaling in Gastric Cancer

Cited by 176 publications

References 188 publications

Gastroprotective Effects of Fermented Lotus Root against Ethanol/HCl-Induced Gastric Mucosal Acute Toxicity in Rats

Gastroprotective Effects of Fermented Lotus Root against Ethanol/HCl-Induced Gastric Mucosal Acute Toxicity in Rats

Nuclear factor‐kappa β as a therapeutic target for Alzheimer's disease

<p>The LINC00365/SCGB2A1 (Mammaglobin B) Axis Down-Regulates NF-κB Signaling and Is Associated with the Progression of Gastric Cancer</p>

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