Effect of interleukin-1β and tumor necrosis factor α gene silencing on mouse gastric cancer cell proliferation and migration

Sun, Zhongwei; Yue, Meng; Liu, Guoqin; Jiang, Yongsheng; Meng, Qinghua; Hu, Sanyuan

doi:10.3892/ol.2016.4253

Cited by 7 publications

(5 citation statements)

References 39 publications

(39 reference statements)

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“…According to research on renal cell carcinoma, small doses of TNF-α in the tumor microenvironment can enhance tumor cell proliferation, invasion, and metastasis, increase white blood cells, form blood vessels, and induce upregulation of other cytokines (e.g., angiogenesis factor and matrix metalloproteinases), and trigger epithelial-mesenchymal transition (EMT) of tumor cells [ 7 ]. In addition, an animal experiment also found that silencing the TNF-α gene can inhibit the proliferation and migration of gastric cancer cells [ 8 ]. Nevertheless, how TNF-α promotes invasion and metastasis of tumor cells is unclear.…”

Section: Introductionmentioning

confidence: 99%

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Tang

Tao

Fang

et al. 2017

Med Sci Monit Basic Res

101

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BackgroundRecent evidence reveals that the inflammatory microenvironment is associated with tumor migration, invasion, and metastasis. Tumor necrosis factor-α (TNF-α) play a vital role in regulation of the inflammatory process in tumor development. Nuclear factor-kappa B (NF-κB) is one of the key transcription factors which regulate processes in tumor promotion. The aim of this study was to explore the role of NF-κB on the invasion and migration of oral squamous cell carcinoma (OSCC).Material/MethodsThe IKKβ and p65 mRNA and protein levels were determined by quantitative RT-PCR and western blot. Wound scratch healing assays and transwell migration assays were used to evaluate the effect of TNF-α and BAY11-7082 on the migration of the OSCC cell lines (HN4, HN6, and CAL27).ResultsWe observed a significant increase of the expression level of IKKβ and p65 in OSCC cells from the experimental group at 24 h, 48 h, and 72 h after TNF-α stimulation. Invasion and metastasis of OSCC cells was obviously improved after the TNF-α stimulation. Invasion and metastasis ability of OSCC cells was inhibited in the suppression group, and no significant changes were observed in expression level of IKKβ and p65 after the use of BAY11-7082.ConclusionsOur results suggest that TNF-α enhances the invasion and metastasis ability of OSCC cells via the NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Tang

Tao

Fang

et al. 2017

Med Sci Monit Basic Res

101

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“…It has been reported that IL-6 is a pivotal target of metformin that can inhibit cancer growth and metastasis [17]. The inhibition of IL-1β and IL-18 by metformin also plays an important role in suppressing gastric tumorigenesis because IL-1β can stimulate gastric cancer cell proliferation and IL-18 can facilitate gastric cancer cell immune escape [44,45]. In addition, TNF-α, which induces insulin resistance in type 2 diabetes, also promotes gastric cancer proliferation, migration, and invasion [44].…”

Section: Discussionmentioning

confidence: 99%

“…The inhibition of IL-1β and IL-18 by metformin also plays an important role in suppressing gastric tumorigenesis because IL-1β can stimulate gastric cancer cell proliferation and IL-18 can facilitate gastric cancer cell immune escape [44,45]. In addition, TNF-α, which induces insulin resistance in type 2 diabetes, also promotes gastric cancer proliferation, migration, and invasion [44]. Our study shows that expression of TNF-α mRNA is decreased by 62 % in db/ db mice treated with metformin.…”

Section: Discussionmentioning

confidence: 99%

Metformin Inhibits N-Methyl-N-Nitrosourea Induced Gastric Tumorigenesis in db/db Mice

Zhuang

Jian

Sun

2017

Exp Clin Endocrinol Diabetes

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Type 2 diabetes can elevate risk of gastric cancer and metformin, an anti-diabetic agent, has an inhibitory effect against gastric cancer cell in vitro. However, the effect of metformin on type 2 diabetes-related gastric tumorigenesis in vivo is still not clear. In the present study, we aim to detect whether metformin can inhibit increased risk of gastric cancer in diabetic db/db mice and which the potential anti-cancer mechanisms of metformin are. 4-week-old mice were divided into 3 groups (2 db/db mice groups and one wild type mice group). All diabetic and non-diabetic mice were treated with N-Methyl-N-Nitrosourea (MNU) for 20 weeks to induce gastric tumorigenesis. At week 21, one db/db mice group were treated with metformin (5 mg/ml) for 10 weeks and the other 2 groups were treated with saline. Blood samples were collected for testing insulin and insulin-like growth factor (IGF)-1. Stomach tissues were collected for histopathological evaluation and mRNAs analysis. Metformin significantly decreased incidence of MNU-induced gastric dysplasia and cancer in diabetic db/db mice. Furthermore, metformin reduced serum insulin as well as IGF-1, and also suppressed expression of insulin receptor, IGF-1, IGF-1 receptor and several pro-inflammatory cytokines mRNAs in stomach of db/db mice, but did not significantly influence IGF-2 and IGF-2 receptor expressions. The results show that metformin can prevent the risk of gastric cancer in type 2 diabetes and the protective mechanisms may involve in an inhibitory effect of metformin on insulin as well as IGF-1 signals and cancer related pro-inflammatory cytokines.

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“…Regarding the ability of OSCC to invade and metastasize or be enhanced by the presence of inflammatory mediators [ 46 , 47 ], TNF-α is worthy of particular attention in OSCC, with its presence demonstrated to enhance cell proliferation and its downregulation demonstrated to inhibit proliferation and migration in other carcinomas, both in vitro [ 48 ] and in vivo animal models [ 49 ].…”

Section: The Role Of Tnf-α In the Promotion Of Osccmentioning

confidence: 99%

Tumour Necrosis Factor Alpha (TNF-α) and Oral Squamous Cell Carcinoma

Brierly

Celentano

Breik

et al. 2023

Cancers

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Uncovering the inflammatory mechanisms underpinning initiation, progression, and promotion of oral squamous cell carcinoma (OSCC) development is fundamental to the rational pursuit of targeted therapeutics. Here we present a review of the current knowledge of the role of TNF-α in the aetiology, pathogenesis, and potential therapies with regards to OSCC. TNF-α is worthy of particular attention in OSCC, with its presence demonstrated to enhance cell proliferation and its downregulation demonstrated to inhibit proliferation and migration in other carcinomas in both in vitro and in vivo models and oral cancer patients. Increased TNF-α in the OSCC tumour microenvironment has been demonstrated to favour invasion through promotion of firstly the pro-inflammatory, pro-invasive phenotypes of OSCC cells and secondly its paracrine mechanism mediating recruitment and activation of inflammatory cells. Polymorphisms affecting the gene expression of TNF-α have been strongly associated with an increased risk for oral squamous cell carcinoma. A number of studies have considered TNF-α within biofluids, including saliva and serum, as a potential biomarker for the early detection of OSCC, as well as its staging, differentiation, and prognosis. The broad and multifaceted role that TNF-α plays in many inflammatory states presents an obvious confounder, particularly with demonstrated increased TNF-α levels in common oral disease states. Lastly, biologic agents targeting TNF-α are currently in clinical use for immune-mediated inflammatory rheumatological and gastrointestinal diseases. There is the potential that these biological agents might have an adjunctive role in OSCC prevention and treatment.

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Effect of interleukin-1β and tumor necrosis factor α gene silencing on mouse gastric cancer cell proliferation and migration

Cited by 7 publications

References 39 publications

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

TNF-Alpha Promotes Invasion and Metastasis via NF-Kappa B Pathway in Oral Squamous Cell Carcinoma

Metformin Inhibits N-Methyl-N-Nitrosourea Induced Gastric Tumorigenesis in db/db Mice

Tumour Necrosis Factor Alpha (TNF-α) and Oral Squamous Cell Carcinoma

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