Tumor necrosis factor receptor superfamily member 14 (TNFRSF14) is dysregulated in certain types of cancer; however, limited data are available on the expression and function of TNFRSF14 in bladder cancer.
The progression of DNA repair and cell proliferation in stage 1 bladder cancer ultimately results not only in the derepression of miR-200a and miR-200b but also in the regulation of the TNF pathway to metastasis-related genes or proteins, cell proliferation, and DNA repair in stage 4 bladder cancer.
Mechanism dissection found ICI 182,780 could promote BCG attachment/internalization to the BCa cells through increased integrin-α5β1 expression and IL-6 release, which may enhance BCG-induced suppression of BCa cell growth via recruiting more monocytes/macrophages to BCa cells and increased TNF-α release.
Genetic variants in the tumor necrosis factor-related apoptosis-inducing ligand and death receptor genes contribute to susceptibility to bladder cancer.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows a strong apoptosis-inducing effect on a variety of cancer cells including bladder cancer.
Association of tumour necrosis factor-alpha gene (T-1031C, C-863A, and C-857T) polymorphisms with bladder cancer susceptibility and outcome after bacille Calmette-Guérin immunotherapy.
In the bladder cancer group, patients with the TNF-beta1 allele had a significantly higher risk for a high-grade tumor (grade 3) or carcinoma in situ (CIS) than those without the TNF-beta1 allele.
Previously we have reported that RT4, a well differentiated human bladder cancer line, increases the expression of macrophage derived chemokine (MDC) and interferon (IFN)-gamma-inducible protein-10 (IP-10) in response to IFN-gamma and tumor necrosis factor (TNF)-alpha.
To determine whether polymorphisms of tumor necrosis factor-alpha (TNF-alpha), vascular endothelial growth factor (VEGF), human 8-oxoguanine DNA glycosylase 1 (hOGG1), glutathione S-transferase-mu (GSTM1), and glutathione S-transferase-phi (GSTT1) are risk factors for bladder cancer among Koreans.
Using the TaqMan method, we genotyped single nucleotide polymorphisms in interleukin (IL) -6 (-174 G-->C), IL-8 (-251 T-->A), tumor necrosis factor-alpha (TNF-alpha; -308 G-->A), and peroxisome proliferator-activated receptor gamma (PPARG; Pro12Ala), and determined their associations with BC initiation and clinical outcome.
To investigate whether the genetic polymorphism of the -308 nucleotide in the tumor necrosis factor-alpha (TNF-alpha) promoter is associated with bladder cancer.
Taken together, these data suggest that most of the cis elements that confer the bladder-specificity and differentiation-dependent expression of the human UPII gene reside in the 2542-bp sequence, and TNFalpha driven by the human UPII (hUPII) promoter is effective in the specific inhibition of bladder cancer growth both in vivo and in vitro.
It was seen that there was a significant association of two polymorphisms in TNF with bladder cancer: the TNF+488A allele was found in 28.1% of patients compared with 14.9% of controls (P=0.0012).
Furthermore, this diverse response of bladder cancer cells to TNF-alpha and INF-gamma suggests that BCG immunotherapy may enhance the invasiveness of bladder cancer in certain conditions with induction of MMPs.
Concomitant treatment of MBT-2 bladder tumour by tumour necrosis factor alpha and interferon alpha in conjunction with delayed type hypersensitivity immunotherapy.