Insulin-like growth factor binding protein-3 enhances etoposide-induced cell growth inhibition by suppressing the NF-κB activity in gastric cancer cells

Kim, Min Sun; Lee, Dae-Yeol

doi:10.1007/s11010-015-2341-2

Cited by 12 publications

(3 citation statements)

References 36 publications

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“…Overexpression of IGFBP-3 resulted in significant inhibition of total and phosphorylated RelA and IκB-proteins in gastric cancer cells and in reduced expression of NF-κB-regulated cell adhesion molecules, ICAM-1 and VCAM-1 [129]. …”

Section: Tumor Suppressors and Nf-κb Regulation In Gastric Cancermentioning

confidence: 99%

NF‐κB Signaling in Gastric Cancer

Sokolova

Naumann

2017

Toxins

182

122

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Gastric cancer is a leading cause of cancer death worldwide. Diet, obesity, smoking and chronic infections, especially with Helicobacter pylori, contribute to stomach cancer development. H. pylori possesses a variety of virulence factors including encoded factors from the cytotoxin-associated gene pathogenicity island (cagPAI) or vacuolating cytotoxin A (VacA). Most of the cagPAI-encoded products form a type 4 secretion system (T4SS), a pilus-like macromolecular transporter, which translocates CagA into the cytoplasm of the host cell. Only H. pylori strains carrying the cagPAI induce the transcription factor NF-κB, but CagA and VacA are dispensable for direct NF-κB activation. NF-κB-driven gene products include cytokines/chemokines, growth factors, anti-apoptotic factors, angiogenesis regulators and metalloproteinases. Many of the genes transcribed by NF-κB promote gastric carcinogenesis. Since it has been shown that chemotherapy-caused cellular stress could elicit activation of the survival factor NF-κB, which leads to acquisition of chemoresistance, the NF-κB system is recommended for therapeutic targeting. Research is motivated for further search of predisposing conditions, diagnostic markers and efficient drugs to improve significantly the overall survival of patients. In this review, we provide an overview about mechanisms and consequences of NF-κB activation in gastric mucosa in order to understand the role of NF-κB in gastric carcinogenesis.

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Section: Tumor Suppressors and Nf-κb Regulation In Gastric Cancermentioning

confidence: 99%

NF‐κB Signaling in Gastric Cancer

Sokolova

Naumann

2017

Toxins

182

122

View full text Add to dashboard Cite

show abstract

“…Under normal conditions, NF-κB dimmers bind to inhibitory IκB proteins and remain in the cytoplasm in a latent form as a transcription factor. After stimulation, IκB is phosphorylated, triggering its dissemination and proteasomal degradation, releasing NF-κB for translocation to the nucleus where it is involved in the inflammatory response, including cytotoxic factors (iNOS) and proinflammatory cytokines such as TNF-α, IL-1β, and IL-6, and stimulates transcription of domainspecific target genes (La Rosa et al 1994, Kim & Lee 2015. Remarkably, our results showed that GOS significantly suppressed APAP-induced NF-κB activation.…”

Section: Cinar Et Almentioning

confidence: 50%

Effects of gossypin on acetaminophen-induced hepatotoxicity in mice

Çınar,

Yayla,

Toktay

et al. 2024

Trakya University Journal of Natural Sciences

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Liver injury from paracetamol (acetaminophen) (APAP) is common worldwide. To prevent intoxication with a drug with high poisoning, treatment can be made possible with an easily accessible and harmless substance. This study aimed to investigate the hepatoprotective ef-fects of Gossypin (GOS) in mice exposed to an overdose of APAP -the possible mechanism of action. Specifically, serum [alanine aminotransferase (ALT), aspartate transaminase (AST), and hepatic biochemical parameters (glutathione (GSH), malondialdehyde (MDA) and super-oxide dismutase (SOD)] were evaluated. Protein and mRNA levels of inflammatory, apoptot-ic, and cytochrome factors, including TNF-α, IL-1β, IL-6, NF-kB, and CYP2E1, were ana-lyzed using real-time PCR. Pretreatment with GOS significantly reduced APAP-induced he-patic injury via oxidative stress. Along with potent antioxidant activity, GOS promoted APAP hepatic detoxification by regulating AST, ALT, GSH, MDA, and SOD activities and mRNA levels of the cytochrome CYP2E1 gene. The anti-inflammatory activity of GOS in-creases its production. TNF-α, IL-1β and IL-6, through possible NF-kB blockade, are also responsible for its hepatoprotective effect. Taken together, GOS has the potential to be devel-oped as a preventive agent to be administered to patients suffering from APAP overdose.

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“…IGFBP3 has potential as a drug, and the 16-kDa IGFBP3 fragment could potentiate apoptosis (26)(27)(28). IGFBP3 overexpression enhanced chemotherapy-induced growth inhibition due to inhibiting NF-kB (29). In addition, promoter hypermethylation of IGFBP3 might be a diagnostic and predictive biomarker for colorectal cancer (30,31).…”

Section: Introductionmentioning

confidence: 99%

Insulin-like Growth Factor-1, Insulin-like Growth Factor Binding Protein-3 and the Incidence of Malignant Neoplasms in a Nested Case–Control Study

Adachi

Nojima

Mori

et al. 2020

Cancer Prevention Research

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Insulin-like growth factor (IGF)-1 is a potent mitogen, but IGF binding protein (IGFBP)-3 inhibits IGF1. To elucidate the relationship between both IGF1 and IGFBP and the risk of tumorigenesis, the association between IGF1 and IGFBP3 serum levels and of malignant tumor incidence was investigated in a prospective case-control study nested in the Japan Collaborative Cohort Study. A baseline survey was started in [1988][1989][1990] 110,585 subjects were enrolled, and 35% of participants donated blood samples. Those who had been diagnosed with malignant tumors by 1997 were considered cases. The analysis involved 1,349 cases and 4,012 controls. Conditional logistic regression was used to estimate ORs for cancer incidence associated with IGF-related molecules. After controlling for alcohol intake, body mass index (BMI), and smoking, participants with high total-IGFBP3 and free-IGFBP3, which is estimated by the molar difference of (IGFBP3 À IGF1), had a risk of future neoplasms (P trend ¼ 0.014 and 0.009, respectively), but those with IGF1 did not. People in the second to fifth quintiles had a lower risk than those in the first quintile (ORs 0.676-0.736 and 0.657-0.870, respectively). Limiting subjects to those followed for 3 years weakened the negative associations of total-and free-IGFBP3, whereas a positive relationship of free-IGF1, which was estimated by the molar ratio of IGF1/IGFBP3, was seen (P trend ¼ 0.004, 0.002, and 0.013, respectively). After controlling for alcohol intake, smoking, BMI, and diabetes mellitus, the results were confirmed. These findings suggest that serum IGF1 and IGFBP3 are related to future risk of malignant neoplasms.

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Insulin-like growth factor binding protein-3 enhances etoposide-induced cell growth inhibition by suppressing the NF-κB activity in gastric cancer cells

Cited by 12 publications

References 36 publications

NF‐κB Signaling in Gastric Cancer

NF‐κB Signaling in Gastric Cancer

Effects of gossypin on acetaminophen-induced hepatotoxicity in mice

Insulin-like Growth Factor-1, Insulin-like Growth Factor Binding Protein-3 and the Incidence of Malignant Neoplasms in a Nested Case–Control Study

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