Cellular and humoral immune responses to human urinary bladder carcinomas

Bubenı́k, Jan; Perlmann, Peter; Helmstein, K; Moberger, G.

doi:10.1002/ijc.2910050303

Cited by 259 publications

(36 citation statements)

References 16 publications

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“…The recognition that neutrophils have potential anti-tumor functions was first brought forward in the 1970s where neutrophils from patients with bladder cancer were shown to be cytotoxic toward bladder cancer cells [308]. Since then neutrophils were shown to exert their anti-tumor functions via direct cytotoxicity, antibody dependent cell mediated cytotoxicity (ADCC) and through the presentation of specific antigens (Table 2) [7].…”

Section: Anti-tumor Functions Of Neutrophilsmentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

336

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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Section: Anti-tumor Functions Of Neutrophilsmentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

336

261

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“…T24 is a cell line derived from human urinary bladder transitional epithelial cell carcinoma (Bubenik et al 1970), and was a generous gift from the Department of Urology, Hirosaki University School of Medicine. The cells were cultured using RPMI1640 supplemented with 10% (v/v) FBS.…”

Section: Cell Culturementioning

confidence: 99%

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Imaizumi

Yagihashi²,

Hatakeyama

et al. 2004

Tohoku J. Exp. Med.

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Urinary bladder epithelial cells play an important role in the host defense against urinary tract infections. Interferon-γ (IFN-γ ) is a potent cytokine that regulates immune responses by inducing multiple genes in many types of cells including urinary bladder epithelial cells. Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH-box family, which is involved in various reactions related to RNA metabolism, and is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. We have studied the expression of RIG-I in T24 cells, a cell line derived from human urinary bladder epithelial carcinoma cells. IFN-γ stimulated T24 cells to express RIG-I mRNA and protein in concentration-and time-dependent manners. Immunohistochemical analysis revealed the expression of RIG-I in the urinary bladder epithelium from a patient with chronic urinary tract infection and in a bladder epithelial carcinoma. We conclude that RIG-I may play some role in inflammatory reactions in the urinary tract epithelium.RIG-I; IFN-γ ; T24 cells; urinary bladder epithelial cells

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“…19 ECV304 cell line, a bladder cancer-derived cell line, 26 has been reported to express many endothelial surface antigens, 27,28 among them is Tie2 (Brizzi et al unpublished data). These cells were transfected with the dominant negative STAT5 (⌬STAT5) construct 13 by the lipofectin methods.…”

Section: Cell Cultures and Transfectionsmentioning

confidence: 99%

Angiopoietin 2 Induces Cell Cycle Arrest in Endothelial Cells: A Possible Mechanism Involved in Advanced Plaque Neovascularization

Calvi

Dentelli

Pagano

et al. 2004

ATVB

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Objective-To characterize the molecules and the mechanisms regulating the neoangiogenetic process in advanced atherosclerotic plaques. Methods and Results-Western blot and immunofluorescence analysis of atherosclerotic specimens demonstrated that unlike neovessels from early lesions that expressed vascular endothelial growth factor (VEGF) and angiopoietin1 (Angio1), vessels from advanced lesions expressed VEGF and angiopoietin 2 (Angio2). Moreover, only few neovessels from advanced lesions showed a positive immunostaining for proliferating cell nuclear antigen. Angio1-elicited and Angio2-elicited intracellular events in endothelial cells (EC) demonstrated that while Angio1 triggered Erk1/Erk2 mitogen activated protein kinases (MAPK) and Akt activation, Angio2 (50 ng/mL) induced STAT5 activation and p21 waf expression and increased the fraction of cells in G1. Both Angio2-mediated events were abrogated by expressing a dominant negative STAT5 construct (⌬STAT5). Consistent with the expression of Angio2 in neovessels of advanced lesions a transcriptionally active STAT5 was detected. Moreover, co-immunoprecipitation experiments revealed the presence of a STAT5/Tie2 molecular complex in neointima vessels from advanced, but not from early, lesions. 3 Consistently, in vivo developing primary lesions might be considered as underperfused and dependent on neovessel formation for continued growth. 4 Angiogenesis in mature tissues is composed of a series of cellular responses including activation of EC proliferation by angiogenic factors, such as VEGF, fibroblast growth factor (FGF), and angiopoietins (Angio) and formation of tube-like structures and vessel stabilization. 5 Compared with the developmental angiogenesis, the role of angiopoietins in pathological angiogenesis is less understood. The angiopoietin family consists of four members, Angio1 to 4. 6 -8 Angio1 and 4 stimulate their receptor tyrosine kinase Tie2, whereas Angio2 and 3 by binding to Tie2 antagonize Angio1 signaling. 6 -8 Signal transduction pathways via Tie2 and VEGF receptors (VEGFR) have been extensively examined. 9,10 In particular, Korpelainem et al showed that Tie2 and VEGFR1 overexpression triggers the phosphorylation of the signal transducer and activator of transcription (STAT) 3 and STAT5. 11 STAT5 belongs to the family of transcriptional factors, which, on activation, binds to the receptor via their src homology 2 domain (SH2). 12 Recruited STATs, dimerize, translocate to the nucleus, and activate transcription of target genes mainly involved in regulation of cell cycle progression. 12,13 Cell cycle phases are coordinated by regulatory proteins denoted as cyclins and cyclin-dependent kinases (CDKs). 14 Phase-specific cyclin/CDK complexes confer specificity and orderly progression through the cell cycle. Initially, cyclin D/CDK4 or cyclin E/CDK2 complexes, in cooperation with proliferating cell nuclear antigen (PCNA), coordinate DNA duplication by regulating the transition through the G1 and S phase. 15 Furthermore, cell cycle progression is ...

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Cellular and humoral immune responses to human urinary bladder carcinomas

Cited by 259 publications

References 16 publications

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Angiopoietin 2 Induces Cell Cycle Arrest in Endothelial Cells: A Possible Mechanism Involved in Advanced Plaque Neovascularization

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