Bladder cancer immunogenicity: expression of CD80 and CD86 is insufficient to allow primary CD4+ T cell activation<i>in vitro</i>

Pettit, Stephen; Ali, Simi; O'Flaherty, E; Griffiths, T.R. Leyshon; Neal, David E.; Kirby, John A.

doi:10.1046/j.1365-2249.1999.00857.x

Cited by 12 publications

(11 citation statements)

References 40 publications

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“…In addition, a lower CD80 mRNA level was observed to associate with the more aggressive follicular PTC variant. These findings corroborate previous evidence showing reduced expression of CD80 in many cancer types (i.e., melanoma, myeloma, acute myeloid leukemia, bladder, and colon carcinoma) and are in agreement with the observation of its lower expression in poorer differentiated esophageal cancers, compared to well- and moderate-differentiated ones [ 21 , 52 , 53 ]. Thus, it may be tempting to speculate that reduced CD80 gene expression may confer an advantage to tumor growth.…”

Section: Discussionsupporting

confidence: 92%

CTLA-4 and PD-1 Ligand Gene Expression in Epithelial Thyroid Cancers

Tuccilli

Baldini

Sorrenti

et al. 2018

International Journal of Endocrinology

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The dysregulation of PD-1 ligands (PD-L1 and PD-L2) and CTLA-4 ligands (CD80 and CD86) represents a tumor strategy to escape the immune surveillance. Here, the expression of PD-L1, PD-L2, CD80, and CD86 was evaluated at the mRNA level in 94 patients affected by papillary thyroid carcinoma (PTC) and 11 patients affected by anaplastic thyroid carcinoma (ATC). Variations in the mRNAs in PTC patients were then correlated with clinicopathological features. The expression of all genes was deregulated in PTC and ATC tissues compared to normal tissues. In particular, the downregulation of CD80 was observed above all in ATC. In addition, the increased expression of CD80 associated with longer disease-free survival in PTC. Higher expression of PD-L1 associated with the classical histological variant and with the presence of BRAFV600E mutation in PTC. The increased PD-L2 expression correlated with BRAFV600E mutation and lymph node metastasis, while its lower expression correlated with the follicular PTC variant. The latter was also associated with the CD80 downregulation, which was also related to the absence of lymph node metastasis. In conclusion, we documented the overall dysregulation of PD-1 and CTLA-4 ligands in PTC and ATC tissues and a possible prognostic value for CD80 gene expression in PTC.

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Section: Discussionsupporting

confidence: 92%

CTLA-4 and PD-1 Ligand Gene Expression in Epithelial Thyroid Cancers

Tuccilli

Baldini

Sorrenti

et al. 2018

International Journal of Endocrinology

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“…We focused on the immune response-related genes that negatively correlated with CD147 in CCLE and had been reported previously to express in cancer cells. Finally we selected CD80 [ 31 , 32 ], CD40LG [ 33 ], CD86 [ 31 ] and TNFRSF8 [ 34 , 35 ] for further study ( Supplementary Table 1 ). Notably, silence of CD147, the mRNA expression of the four immune response-related genes in NCI-H460 cells, CD80 and CD40LG in Huh-7 cells, and CD80 and CD86 in MDA-MB-231 cells was increased (Figure 4A–4E ).…”

Section: Resultsmentioning

confidence: 99%

System analysis of the regulation of the immune response by CD147 and FOXC1 in cancer cell lines

Shang

Liu

et al. 2018

Oncotarget

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CD147, encoded by BSG, is a highly glycosylated transmembrane protein that belongs to the immunological superfamily and expressed on the surface of many types of cancer cells. While CD147 is best known as a potent inducer of extracellular matrix metalloproteinases, it can also function as a key mediator of inflammatory and immune responses. To systematically elucidate the function of CD147 in cancer cells, we performed an analysis of genome-wide profiling across the Cancer Cell Line Encyclopedia (CCLE). We showed that CD147 mRNA expression was much higher than that of most other genes in cancer cell lines. CD147 varied widely across these cell lines, with the highest levels in the ovary (COLO704) and stomach (SNU668), intermediate levels in the lung (RERFLCKJ, NCIH596 and NCIH1651) and lowest levels in hematopoietic and lymphoid tissue (UT7, HEL9217, HEL and MHHCALL3) and the kidney (A704 and SLR20). Genome-wide analyses showed that CD147 expression was significantly negatively correlated with immune-related genes. Our findings implicated CD147 as a novel regulator of immune-related genes and suggest its important role as a master regulator of immune-related responses in cancer cell lines. We also found a high correlation between the expression of CD147 and FOXC1, and proved that CD147 was a direct transcriptional target of FOXC1. Our findings demonstrate that FOXC1 is a novel regulator of CD147 and confirms its role as a master regulator of the immune response.

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“…Without an effective anti-tumour immune response, these cells may induce tumorigenesis and metastasis via inhibition of the immune response of local tumours. Immune cells in the tumour microenvironment are immunological effector cells that serve an important role in tumour recognition and immune defence to attack tumour cells ( 28 – 30 ). However, it was demonstrated that tumour cells are able to secrete a number of inhibitors, modify antigens on the cell surface, or negatively regulate gene expression so as to escape immune cell recognition and destruction.…”

Section: Discussionmentioning

confidence: 99%

EGFR may participate in immune evasion through regulation of B7‑H5 expression in non‑small cell lung carcinoma

Dong

Zhang

et al. 2018

Mol Med Report

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Lung cancer is one of the most prevalent malignancies worldwide; it has been ranked the most lethal type of cancer. Non-small cell lung carcinoma (NSCLC) comprises >80% of all types of lung cancer. Although certain achievements have been made in the treatment of NSCLC, including the targeted gene drug epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), the five-year survival rate of patients has not significantly increased. A previous study demonstrated that B7-H5, a novel co-stimulatory molecule in the B7 molecule family, was negatively correlated with EGFR in pancreatic cancer. Thus, in the present study, we aimed to investigate whether EGFR participates in immune evasion, probably through regulation of B7-H5 expression. NCI-H1299 NSCLCL cells were divided into control, mock, small interfering-EGFR and EGFR-TKI groups. The cell viability and apoptosis rate were analysed by a Cell Counting Kit-8 assay and flow cytometry. The transforming growth factor (TGF)-β and interleukin (IL)-10 content was measured using an ELISA. The expression levels of EGFR, B7-H5, Survivin, apoptosis regulator Bax, apoptosis regulator Bcl-2 (Bcl-2), TGF-β, vascular endothelial growth factor (VEGF), IL-10 and cyclooxygenase (COX)-2 were assessed via quantitative PCR and western blotting. The activation of the tyrosine-protein kinase JAK2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signalling pathway was detected using western blotting. The results demonstrated a notable negative correlation between EGFR and B7-H5 expression levels in cancer tissues and cell lines. Inhibition of EGFR expression via gene silencing and EGFR inhibition markedly decreased cell viability and increased the apoptosis of NCI-H1299 cells, by upregulating survivin and Bcl-2 expression. The protein expression levels of TGF-β, VEGF, IL-10 and COX-2 were additionally decreased, with weak activation of the JAK2/STAT3 signalling pathway. EGFR may be involved in immune evasion, possibly through regulation of B7-H5 expression in NSCLC.

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Bladder cancer immunogenicity: expression of CD80 and CD86 is insufficient to allow primary CD4+ T cell activationin vitro

Cited by 12 publications

References 40 publications

CTLA-4 and PD-1 Ligand Gene Expression in Epithelial Thyroid Cancers

CTLA-4 and PD-1 Ligand Gene Expression in Epithelial Thyroid Cancers

System analysis of the regulation of the immune response by CD147 and FOXC1 in cancer cell lines

EGFR may participate in immune evasion through regulation of B7‑H5 expression in non‑small cell lung carcinoma

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