Interferon regulatory factor‐1 is prerequisite to the constitutive expression and IFN‐γ‐induced upregulation of B7‐H1 (CD274)

Lee, Seung Jin; Jang, Byeong Churl; Lee, Soo Woong; Yang, Young Il; Suh, Seong Il; Park, Yeong Min; Oh, Sangtaek; Shin, Jae Gook; Yao, Sheng; Chen, Lieping; Choi, In Taek

doi:10.1016/j.febslet.2005.12.093

Cited by 410 publications

(387 citation statements)

References 26 publications

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“…The observation that INF␥ and Toll-like receptors enhance persistent expression of CD274 in malignant plasma cells by acting via the MyD88, TRAF6, and MAPK signaling pathways (31) supports this conclusion. Finally, the IRS-1 transcription factor has been found to activate the CD274 gene in the lung carcinoma cell line (30). Whether IRS-1 and STAT3 act independently or can cooperate in inducing CD274 expression in at least some types of normal and malignant cells remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1)

Marzec

Zhang²,

Goradia³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

624

484

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Section: Discussionmentioning

confidence: 99%

Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1)

Marzec

Zhang²,

Goradia³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

624

484

View full text Add to dashboard Cite

“…The induction of B7-H1 molecule in the current primary cell lines is not dependent on inflammatory cytokines (g-IFN and TNF-a) known to induce B7-H1. [37][38][39] The similarity in the expression of B7-H1 in fibroblasts and epithelial cell cultures, obtained form either normal or tumor tissues, suggests that B7-H1 is directly related to proliferation and not tumorgenesis (cell transformation). Similarly, Parsa et al have recently found that expression of B7-H1 in human astrocytes was dependent on Akt activation but not on cellular immortalization or transformation.…”

Section: Discussionmentioning

confidence: 99%

Expression of B7‐H1 in breast cancer patients is strongly associated with high proliferative Ki‐67‐expressing tumor cells

Ghebeh¹,

Tulbah²,

Mohammed³

et al. 2007

Intl Journal of Cancer

132

106

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B7-H1, a coinhibitory molecule, plays a role in immune escape of tumors. We have shown previously the expression of this molecule in breast cancer patients and demonstrated its association with high histological grade, progesterone and estrogen receptor negative status, all of which are known to have direct impact on cell proliferation. In the present work, we investigated the effect of proliferation, as measured by Ki-67 and mitotic count, on the induction of B7-H1. We used H&E stained sections to score for mitotic count in 69 breast cancer patients. Immunohistochemistry was used to investigate B7-H1 and Ki-67 expression. The relationship between B7-H1 induction and cell proliferation was further investigated in primary cultured cells. B7-H1 expression was recorded in patients with a high mitotic index (p 5 0.007). There was a high significant correlation between B7-H1 expression and the presence of the proliferative marker Ki-67 (p < 0.001) indicating the association of proliferation with B7-H1 induction. Furthermore, B7-H1 was gradually induced in proliferating cells of 8/8 primary cell lines as measured by Ki-67 expression. Finally, B7-H1 was downregulated in quiescent cells and upregulated in cells stimulated with a mitogen confirming the association of proliferation with the induction of B7-H1. We have shown for the first time a direct association between proliferation and the expression of B7-H1 in breast cancer patients. The relationship between B7-H1 induction and cell proliferation was also thoroughly investigated in vitro, in which a strong link between B7-H1 expression and the presence of the proliferative Ki-67 marker was clearly demonstrated. ' 2007 Wiley-Liss, Inc.Key words: B7-H1; PD-L1; breast cancer; Ki-67; proliferation; mitotic index About 40% of women still die of breast cancer in spite of the significant advances in traditional, targeted and neo-adjuvant therapies. 1 Immunotherapeutic strategies aimed at manipulating the patient's immune system to specifically destroy tumor cells may represent a major alternative approach for the management of cancer. 2,3 However, the presence of an existing immune tolerance in patients with advanced cancer may limit the clinical effectiveness of such therapeutic strategies. 4 Several mechanisms have been attributed to the immune defect seen in breast cancer patients with advanced disease; where a lower number of blood lymphocytes, 5 elevated T regulatory lymphocytes, 6 defective dendritic cells 7 and expression of FasL in breast cancer 8 were described.A T lymphocyte inhibitory molecule named B7-H1 (also called PD-L1) expressed by antigen presenting cells has been shown to induce T lymphocyte anergy and/or apoptosis after ligation to its T lymphocytes receptor PD-1. 9-12 It has been shown to be directly involved in the protection of cancer cells from activated T lymphocytes. 13 The expression of this molecule has been described in several malignancies including ovary, colon, melanoma and carcinoma of the lung. 11 Others includes; squamous cell carcinoma o...

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“…To further explore the possible mechanism of IL-12 exerts function in regulating B7-H1 expression; we investigated the expression of IFN-γ firstly, because IFN-γ has been well known to induce the expression of B7-H1 (Lee et al, 2005;Lee et al, 2006;Kondo et al, 2010). It was found that rIL-12 and Ad-IL-12-GFP treated groups produced a higher level of IFN-γ in the supernatants of monocyte-derived macrophages cocultured with SKOV3 system.…”

Section: Il-12 Increased the Level Of Ifn-γ And Decreased The Level Omentioning

confidence: 99%

IL-12 Regulates B7-H1 Expression in Ovarian Cancer-associated Macrophages by Effects on NF-κB Signalling

Xiong¹,

Ma²,

Wu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Interferon regulatory factor‐1 is prerequisite to the constitutive expression and IFN‐γ‐induced upregulation of B7‐H1 (CD274)

Cited by 410 publications

References 26 publications

Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1)

Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1)

Expression of B7‐H1 in breast cancer patients is strongly associated with high proliferative Ki‐67‐expressing tumor cells

IL-12 Regulates B7-H1 Expression in Ovarian Cancer-associated Macrophages by Effects on NF-κB Signalling

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