Inflammation, a Key Event in Cancer Development

Lu, Haitian; Ouyang, Wei; Huang, Chuanshu

doi:10.1158/1541-7786.mcr-05-0261

Cited by 946 publications

(792 citation statements)

References 207 publications

(297 reference statements)

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“…It may be a good model of inflammation-associated carcinogenesis, because H. pylori infection induces intense acute and chronic inflammatory reaction that may last for decades (Price, 1991;Dixon et al, 1996). Moreover, H.pylori infection, environmental exposures, host genetic susceptibility, or some combination of these factors can lead to increased expression of cytokines, growth factors and their receptors, which in turn promotes cellular proliferation (Coussens and Werb, 2002;Lu et al, 2006). In addition, free radicals are generated as by-products of the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

SNPs of Excision Repair Cross Complementing Group 5 and Gastric Cancer Risk in Chinese Populations

Yang¹,

Zhang²,

Chen³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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We conducted a case-control study to determine the association between several potential SNPs of excision repair cross complementing group 5 (XPG) and gastric cancer susceptibility, and roles of XPG polymorphisms in combination with H.pylori infection in determining risk of gastric cancer. In our study, we collected 337 newly diagnosed gastric cancer cases and 347 health controls. Three SNPs of XPG, rs2296147T>C, rs2094258C>T and rs873601G>A, were genotyped using the Taqman real-time PCR method with a 7900 HT sequence detector system. H. pylori infection was diagnosed by ELISA. By multivariate logistic regression analysis, the rs2296147 CC genotype was associated with a decreased risk of gastric cancer (OR=0.52, 95% CI=0.27-0.97), and rs2094258 TT was associated with elevated risk (OR=2.13, 95% CI=1.22-3.35). Positive H.pylori individuals with rs2094258 TT genotypes demonstrated increased risk of gastric cancer (OR=2.13, 95% CI=1.22-3.35), while rs2296147 CC was associated with lower risk among patients with negative H.pylori (OR=0.45, 95%CI=0.22-0.89). Our findings suggested that XPG polymorphisms might contribute to risk of gastric cancer among Chinese populations, but the effect needs to be further validated by larger sample size studies.

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Section: Discussionmentioning

confidence: 99%

SNPs of Excision Repair Cross Complementing Group 5 and Gastric Cancer Risk in Chinese Populations

Yang¹,

Zhang²,

Chen³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Elevated concentrations of H 2 O 2 , dependent upon diet, lifestyle, and other health factors (Halliwell et al, 2000), can be found in the bladder and lower urinary tract. Epidemiological studies indicate that chronic inflammatory diseases are associated with an increased risk of human malignancies (Lu et al, 2006), including bladder cancer (BlCa) (La Vecchia et al, 1991;Hofseth et al, 1996) and chemical toxicity/irritation.…”

Section: Include (−)-Epicatechin (Ec) and (−)-Epigallocatechin (Egc)mentioning

confidence: 99%

Antioxidant effects of green tea and its polyphenols on bladder cells

et al. 2008

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Genitourinary tract inflammation/ailments affect the quality of life and health of a large segment of society. In recent years, studies have demonstrated strong anti-oxidant effects of green tea and its associated polyphenols in inflammatory states. This in vitro study examined the antioxidant capabilities (and putative mechanisms of action) of green tea extract (GTE), polyphenon-60 (PP-60, 60 % pure polyphenols), (−)-epicatechin-3-gallate (ECG) and (−)-epigallocatechin-3-gallate (EGCG) in normal/malignant human bladder cells following catechin treatment ± 1 mM H 2 O 2 (oxidative agent). Cell viability, apoptosis and reactive oxygen species (ROS) formation were evaluated. Our results showed that H 2 O 2 exposure significantly reduced normal (UROtsa) and highgrade (TCCSUP, T24) bladder cancer (BlCa) cell viability compared with control-treated cells (p < 0.001). No affect on low-grade RT4 and SW780 BlCa cell viability was observed with exposure to H 2 O 2 . Compared to H 2 O 2 -treated UROtsa, treatment with PP-60, ECG and EGCG in the presence of H 2 O 2 significantly improved UROtsa viability (p < 0.01), with strongest effects evoked by ECG. Additionally, though not as effective as in UROtsa cells, viability of both high-grade TCCSUP and T24 BlCa cells, in comparison to H 2 O 2 -treated cells, were significantly improved (p < 0.01) by treatment with PP-60, ECG, and EGCG in the presence of H 2 O 2 . Overall, our findings demonstrate that urothelium cell death via H 2 O 2 -induced oxidative stress is mediated, in part, through superoxide (O 2 −· ), and potentially, direct H 2 O 2 mechanisms, suggesting that green tea polyphenols can protect against oxidative stress/damage and bladder cell death.

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“…In the tumor microenvironment, various inflammatory cells, such as tumor-associated macrophages, are recruited to form a pro-tumor inflammatory environment. Inflammatory cells produce a variety of mediators, including growth factors, chemokines and cytokines, which induce tumor growth, invasion, and angiogenesis (5,6).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β activates focal adhesion kinase and Src to induce matrix metalloproteinase-9 production and invasion of MCF-7 breast cancer cells

2016

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Abstract. Interleukin-1β (IL-1b) is a pleiotropic cytokine that is important in tumor progression and invasion. Matrix metalloproteinase-9 (MMP-9), which is a secreted matrix-degrading enzyme, is one of the key regulators of tumor invasion and metastasis. The current report indicated that IL-1b promotes MMP-9 production and cell invasion in non-metastatic MCF-7 breast cancer cells. IL-1b activated focal adhesion kinase (FAK) and proto-oncogene tyrosine-protein kinase Src (Src). Moreover, inhibiting the Src/FAK pathway reduced the IL-1b-induced production of MMP-9 and cell invasion. To investigate the functional role of FAK in MMP-9 production cell lines expressing mutant FAK in FAK knock-out mouse fibroblasts were generated. In wild-type FAK-expressing cells, MMP-9 production was induced by IL-1b stimulation. By contrast, IL-1b-induced MMP-9 production was abrogated in FAK knock-out, FAK Y397F, FAK Y925F, and kinase dead mutant-expressing cells. Therefore the results of the current study indicate that FAK and Src kinases are activated by IL-1b and play a critical role in MMP-9 production and tumor cell invasion.

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Inflammation, a Key Event in Cancer Development

Cited by 946 publications

References 207 publications

SNPs of Excision Repair Cross Complementing Group 5 and Gastric Cancer Risk in Chinese Populations

SNPs of Excision Repair Cross Complementing Group 5 and Gastric Cancer Risk in Chinese Populations

Antioxidant effects of green tea and its polyphenols on bladder cells

Interleukin-1β activates focal adhesion kinase and Src to induce matrix metalloproteinase-9 production and invasion of MCF-7 breast cancer cells

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