Disease relevance of TNFAIP8

• Western blotting using an antipeptide antibody revealed endogenous SCC-S2 as a approximately 21 kDa cytosolic protein in human breast cancer cells (MDA-MB 231) and renal carcinoma cells (RCC-RS) [1].
• In this study, we examined the role of SCC-S2 in invasion and experimental metastasis [2].
• Forty patients (89%) showed glomerular grade 1 (GG1) and 5 patients (11%) showed GG2, but this grading did not correlate with disease progression [3].
• Using chronicity-based histologic grading, 50, 59, and 35 patients were glomerular grade (GG) 1a, GG1b, and GG2; 83 and 61 patients were tubulointerstitial grade (TIG) 1 and TIG2; and 25 patients had hyaline arteriolosclerosis [4].

High impact information on TNFAIP8

• Inhibition of the GG2-1 gene using the siRNA technique resulted in significantly enhanced apoptosis, decreased proliferation, and decreased production of MMP-1 in TNFalpha-stimulated RASFs [5].
• RESULTS: Blocking of NF-kappaB by AdIkappaB-DN was associated with a down-modulation of antiapoptosis genes, including BIRC-3, and several novel genes, including GG2-1, a TNFalpha-inducible FLIP-like gene [5].
• The steady state level of SCC-S2 mRNA is significantly induced by TNF-alpha in different tumor cells (TNF-alpha at 20 ng/ml for 3 h: A549, approximately 2-9-fold; SKOV-3, approximately 3-fold; PCI-04A, approximately 3-6-fold) [6].
• These data implicate a role of SCC-S2 as a negative mediator of apoptosis in certain cell types [6].
• Based on the nucleotide sequence, the SCC-S2 open reading frame contains a sequence in the amino terminus that shows a significant homology to death effector domain II of cell death regulatory protein, Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (FLIP) [6].

Biological context of TNFAIP8

• Identification of a novel tumor necrosis factor-alpha-inducible gene, SCC-S2, containing the consensus sequence of a death effector domain of fas-associated death domain-like interleukin- 1beta-converting enzyme-inhibitory protein [6].
• SCC-S2 transfectants also displayed an increase in cell migration in collagen I as compared to control transfectants ( approximately twofold; n=3; P<0.005) [1].
• Here we have examined a role of SCC-S2 in cell growth regulation in vitro and in vivo [1].
• MDA-MB 435 human cancer cells stably transfected with the FLAG-tagged SCC-S2 cDNA exhibited increased growth rate as compared to control vector transfectants, as measured by the cell viability (>twofold; n=3; P<0.005) and thymidine-labeling procedures ( approximately sixfold; n=3; P<0.0001) [1].
• These results demonstrate a novel role for SCC-S2 in tumor progression, involving multiple effectors, and provide a basis for SCC-S2-targeted cancer gene therapy [2].

Anatomical context of TNFAIP8

• TNF-alpha treatment (100 ng/ml, 4 h) of HeLa cells transiently transfected with FLAG epitope-tagged SCC-S2 cDNA or expression vector alone led to an increase in the number of apoptotic cells as compared with the untreated counterpart [6].
• Antisense inhibition of endogenous SCC-S2 expression correlated with decreased expression of VEGF receptor-2 in tumor cells and human lung microvascular endothelial cells and loss of endothelial cell viability [2].

Associations of TNFAIP8 with chemical compounds

• Differential regulation of the human insulin gene transcription by GG1 and GG2 elements with GG- and C1-binding factors [7].

Analytical, diagnostic and therapeutic context of TNFAIP8

• The immunofluorescence detection method showed the cytosolic localization of FLAG-tagged human SCC-S2 in COS-1 transfectants [1].

References