Role of SCC-S2 in Experimental Metastasis and Modulation of VEGFR-2, MMP-1, and MMP-9 Expression

Zhang, Chuanbo; Chakravarty, Debyani; Sakabe, Isamu; Mewani, Rajshree R.; Boudreau, Howard E.; Kumar, Deepak; Ahmad, Imran; Kasid, Usha N.

doi:10.1016/j.ymthe.2005.11.020

Cited by 89 publications

(86 citation statements)

References 44 publications

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“…29 It is also a risk factor for non-Hodgkin's lymphoma, and high levels of TNFAIP8 expression are associated with more aggressive forms of epithelial ovarian cancer with poor survival rates 22,30 as well as with non-small cell lung cancer (NSCLC). 31 Furthermore, the overexpression of TNFAIP8 protein in the MDA-MB 435 human breast cancer cell line resulted in increased cell proliferation and cell migration, 17 which was demonstrated to enhance tumorgenicity 32 when injected in athymic mice. In contrast, antisense inhibition in athymic mice resulted in a decreased incidence of pulmonary metastasis.…”

Section: Introductionmentioning

confidence: 99%

“…35 Mechanistic studies have shown that decreased TNFAIP8 expression led to concomitant decreases in the levels of vascular endothelial growth factor receptor-2 (VEGFR-2) and matrix metalloprotease (MMP) 1 and 9. 32 In addition, TNFAIP8 has been shown to be directly coupled to Gαi g-proteins; this interaction does not appear to be involved in Gαi3-mediated cAMP inhibition but is involved in Gi-mediated inhibition of cell death, presumably via the Gβγ subunit. 36 TNFAIP8 protein has also been found to associate with activated RAC1-GTP at the cell membrane, 37 and the knockout of this protein resulted in resistance to lethal Listeria monocytogenes infection via decreased RAC1-mediated cell invasion and increased apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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The TIPE (tumor necrosis factor-α-induced protein 8-like) family are newly described regulators of immunity and tumorigenesis consisting of four highly homologous mammalian proteins: TNFAIP8 (tumor necrosis factor-α-induced protein 8), TIPE1 (TNFAIP8-like 1, or TNFAIP8L1), TIPE2 (TNFAIP8L2) and TIPE3 (TNFAIP8L3). They are the only known transfer proteins of the lipid secondary messengers PIP2 (phosphatidylinositol 4,5-bisphosphate) and PIP3 (phosphatidylinositol 3,4,5-trisphosphate). Cell-surface receptors, such as G-protein-coupled receptors and receptor tyrosine kinases, regulate inflammation and cancer via several signaling pathways, including the nuclear factor (NF)-κB and phosphoinositide-3 kinase (PI3K) pathways, the latter of which is upstream of both Akt and STAT3 activation. An expression analysis in humans demonstrated that the TIPE family is dysregulated in cancer and inflammation, and studies both in mice and in vitro have demonstrated that this family of proteins plays a critical role in tumorigenesis and inflammatory responses. In this review, we summarize the current literature for all four family members, with a special focus on the phenotypic manifestations present in the various knockout murine strains, as well as the related cell signaling that has been elucidated to date.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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“…Human breast cancer cells transfected with TNFAIP8 increased proliferation, cell migration, and tumor growth rate (Kumar et al, 2004). Knocking down of TNFAIP8 expression in tumor cells reduces their tumorigenicity, suggesting that it may play a role in oncogenesis (Zhang et al, 2006). However, it is not known whether TNFAIP8 takes a part in the progress of PC, and if so, what role it may play.…”

Section: Introductionmentioning

confidence: 99%

Expression of Tumor Necrosis Factor-alpha-induced Protein 8 in Pancreas Tissues and its Correlation with Epithelial Growth Factor Receptor Levels

Liu¹,

Qin²,

Wang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 or TIPE) is a recently identified protein considered to be associated with carcinogenesis. To investigate its expression pattern in pancreatic cancer patients and to analyse its correlation with clinicopathological significance and the expression levels of epithelial growth factor receptor (EGFR), immunohistochemistry was performed to detect the TNFAIP8 and EGFR proteins in pancreatic cancers, pancreatitis tissues, and healthy controls. The results showed stronger staining of TNFAIP8 protein in pancreatic cancer tissues compared with normal pancreas tissue. Furthermore, in 56 patients with pancreatic cancer, the expression levels of TNFAIP8 in patients with low tumor stage was higher than that with high tumor stage, and correlated with tumor staging and lymph node metastasis (P<0.05). Furthermore, TNFAIP8 expression positively correlated with EGFR levels (r=0.671135, P<0.05). These results indicate that TNFAIP8 may play important roles in the progression of pancreatic cancer.

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“…The last exon is common, whereas usage of other exons differs across variants (Supplementary Figure S1). Several reports have shown that TNFAIP8 is overexpressed in human cancers, [3][4][5]8,[19][20][21][22] yet none of these publications have used methods with adequate specificity to discriminate among Abbreviations: BrdU, 5-bromo-2'-deoxyuridine; ChIP-seq, chromatin immunoprecipitation sequencing; DOX, doxorubicin; Gadd45A, growth arrest and DNA damageinducible 45a; H3K4me1, histone H3 mono-methylation on lysine 4; H3K4me3, histone H3 tri-methylation on lysine 4; H3K27ac, histone H3 acetylation on lysine 27; p53RE, p53 response element; PCNA, proliferating cell nuclear antigen; Scri, cells expressing scrambled shRNA; shRNA, short hairpin RNA; TCGA, The Cancer Genome Atlas; TNFAIP8, tumor necrosis factor-α-induced protein 8; TP8i, cells expressing TNFAIP8 shRNA …”

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The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

et al. 2016

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Tumor necrosis factor-α-induced protein 8 (TNFAIP8) is a stress-response gene that has been associated with cancer, but no studies have differentiated among or defined the regulation or function of any of its several recently described expression variants. We found that TNFAIP8 variant 2 (v2) is overexpressed in multiple human cancers, whereas other variants are commonly downregulated in cancer (v1) or minimally expressed in cancer or normal tissue (v3-v6). Silencing v2 in cancer cells induces p53-independent inhibition of DNA synthesis, widespread binding of p53, and induction of target genes and p53-dependent cell cycle arrest and DNA damage sensitization. Cell cycle arrest induced by v2 silencing requires p53-dependent induction of p21. In response to the chemotherapeutic agent doxorubicin, p53 regulates v2 through binding to an intragenic enhancer, together indicating that p53 and v2 engage in complex reciprocal regulation. We propose that TNFAIP8 v2 promotes human cancer by broadly repressing p53 function, in essence offsetting p53-dependent tumor suppression. Cell Death and Differentiation (2017) 24, 181-191; doi:10.1038/cdd.2016 published online 11 November 2016 Tumor necrosis factor-α-induced protein 8 (TNFAIP8) is the founding member of a recently described family of environmental stress response genes that are induced by TNFα. TNFAIP8 has been shown to promote or inhibit apoptosis, depending on cell type and context. 1,2 Although little is known about TNFAIP8, it has recently been found to be overexpressed in a wide range of human cancers. Some studies have suggested protumor functions for TNFAIP8, including enhancement of cell survival, proliferation, and metastasis [3][4][5][6][7][8][9] and resistance to cancer chemotherapeutics in mice. 4,10Nonetheless, nothing is known about how TNFAIP8 influences responses to DNA damage in cancer cells. Moreover, several transcript variants from the TNFAIP8 gene were recently registered in the NCBI reference sequence database, but no study to date has differentiated among them or defined the factors that govern their expression.The tumor suppressor p53 is a transcription factor that regulates many biological processes through its target gene network. Some of the well-characterized p53 target genes including p21/CDKN1A, growth arrest and DNA damageinducible 45a (GADD45A) and Bcl-2-like protein 4 (BAX) together promote senescence, cell cycle arrest, and apoptosis, all of which may contribute to the tumor suppressing functions of p53. 11,12Additional noncanonical tumorsuppressive pathways from p53 have recently been identified. [13][14][15] Improved characterization of the p53 DNAbinding sequence with modern sequencing techniques has led to the identification of a rapidly expanding list of p53 target genes. [16][17][18] Continued identification of these genes and characterization of their mechanisms of regulation and function will be critical to a full understanding of p53 and for full realization of opportunities to intervene upon p53 in cancer.Here, we identify ...

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Role of SCC-S2 in Experimental Metastasis and Modulation of VEGFR-2, MMP-1, and MMP-9 Expression

Cited by 89 publications

References 44 publications

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Expression of Tumor Necrosis Factor-alpha-induced Protein 8 in Pancreas Tissues and its Correlation with Epithelial Growth Factor Receptor Levels

The novel p53 target TNFAIP8 variant 2 is increased in cancer and offsets p53-dependent tumor suppression

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