Induced expression of B7-H3 on the lung cancer cells and macrophages suppresses T-cell mediating anti-tumor immune response

Chen, Cheng; Shen, Yu; Qu, Qiuxia; Chen, Xuqin; Zhang, Xueguang; Huang, Jianan

doi:10.1016/j.yexcr.2012.09.006

Cited by 94 publications

(69 citation statements)

References 24 publications

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“…B7-H3 is predominantly expressed in non-hematopoietic tissue [6] but its expression has also been detected in activated lymphocytes in vitro [15] , activated macrophages [16] as well as on endothelial cells of the tumor-associated vasculature [17]. We confirm the notion of a hematopoietic expression of B7-H3 by ex vivo cytometric analysis (Supplementary Fig.…”

Section: Resultssupporting

confidence: 82%

Ablation of B7-H3 but Not B7-H4 Results in Highly Increased Tumor Burden in a Murine Model of Spontaneous Prostate Cancer

Kreymborg

Haak

Murali

et al. 2015

Cancer Immunology Research

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The costimulatory molecules B7-H3 and B7-H4 are overexpressed in a variety of human tumors and have been hypothesized as possible biomarkers and immunotherapeutic targets. Despite this potential, the predominating uncertainty about their functional implication in tumor-host interaction hampers its evaluation as a target for cancer therapy. By means of a highly physiologic, spontaneous tumor model in mice, we establish a causal link between B7-H3 and host tumor control and found B7-H4 to be redundant.

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Section: Resultssupporting

confidence: 82%

Ablation of B7-H3 but Not B7-H4 Results in Highly Increased Tumor Burden in a Murine Model of Spontaneous Prostate Cancer

Kreymborg

Haak

Murali

et al. 2015

Cancer Immunology Research

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show abstract

“…Sun et al reported that B7-H3 expression was positively correlated with a more advanced tumor grade in colorectal cancer [28]. A recent study from Chen et al demonstrated that induced expression of B7-H3 on the lung cancer cells and macrophages suppressed T-cell mediating anti-tumor immune response [29]. Furthermore, it is reported that inhibition of B7-H3 by siRNA significantly suppresses cell migration and invasion, enhances sensitivity to chemotherapeutic drugs in acute monocytic leukemia U937 cells [30].…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3

Liu

et al. 2016

Cell Physiol Biochem

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Background: Chemoresistance is a major obstacle to successful chemotherapy for human non-small cell lung cancer (NSCLC). Astragaloside IV, the component of Astragalus membranaceus, has been reported to exhibit anti-inflammation, anti-cancer and immunoregulatory properties. In the present study, we investigated the role of astragaloside IV in the chemoresistance to cisplatin in NSCLC cells. Methods: We established astragaloside IV-suppressed NSCLC cell lines including A549, HCC827, and NCI-H1299 and evaluated their sensitivity to cisplatin in vitro. In addition, we examined the mRNA and protein levels of B7-H3 in response to cisplatin-based chemotherapy. Results: We showed that high doses of astragaloside IV (10, 20, 40 ng/ml) inhibited NSCLC cell growth, whereas low concentrations of astragaloside IV (1, 2.5, 5 ng/ml) had no obvious cytotoxicity on cell viability. Moreover, combined treatment with astragaloside IV significantly increased chemosensitivity to cisplatin in NSCLC cells. On the molecular level, astragaloside IV co-treatment significantly inhibited the mRNA and protein levels of B7-H3 in the presence of cisplatin. In addition, ectopic expression of B7-H3 diminished the sensitization role of astragaloside IV in cellular responses to cisplatin in NSCLC cells. Conclusion: These results demonstrate that astragaloside IV enhances chemosensitivity to cisplatin via inhibition of B7-H3 and that treatment with astragaloside IV and inhibition of B7-H3 serve as potential therapeutic approach for lung cancer patients.

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“…T cell co-stimulatory effects of B7-H3 have been demonstrated, and theoretically tumours lacking stromal B7-H3 could escape anti-tumour immunity which would otherwise impede disease progression [39, 40]. On the other hand, B7-H3 suppression of anti-tumour immunity has also been reported [18, 41, 42], leaving the immunomodulatory role of B7-H3 in this setting unclear. Another hypothesis could be that stromal B7-H3 restrains disease progression through so far unknown non-immunological mechanisms.…”

Section: Discussionmentioning

confidence: 99%

B7-H3 expression in colorectal cancer: associations with clinicopathological parameters and patient outcome

et al. 2014

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BackgroundWe have previously reported overexpression of the immunoregulatory protein B7-H3 in colorectal cancer and that nuclear expression predicted poor outcome in colon cancer patients. The present study was performed to examine the prognostic role of B7-H3 in an independent colorectal cancer cohort.MethodsUsing tissue microarrays from 731 colorectal cancer patients, tumour B7-H3 expression was assessed by immunohistochemistry. Associations with clinicopathological parameters and patient outcome were investigated.ResultsNuclear expression of B7-H3 in cancer cells was present in 27% of the samples in the total study cohort, while cytoplasmic/membrane and stromal expression was seen in 86% and 77% of the samples, respectively. Nuclear B7-H3 had no prognostic relevance in the complete outcome cohort, neither in colon cancer patients. However, nuclear B7-H3 was significantly associated with reduced recurrence-free survival in TNM stage I colorectal cancer patients.ConclusionsOverexpression of B7-H3 in colorectal cancer was confirmed, but in contrast to previous results, nuclear B7-H3 was not a strong prognostic biomarker in this cohort. The discrepancy might be related to the use of single-core tissue microarrays for detection of the heterogeneously expressed B7-H3, and the role of B7-H3 in colorectal cancer still needs further examination.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2407-14-602) contains supplementary material, which is available to authorized users.

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Induced expression of B7-H3 on the lung cancer cells and macrophages suppresses T-cell mediating anti-tumor immune response

Cited by 94 publications

References 24 publications

Ablation of B7-H3 but Not B7-H4 Results in Highly Increased Tumor Burden in a Murine Model of Spontaneous Prostate Cancer

Ablation of B7-H3 but Not B7-H4 Results in Highly Increased Tumor Burden in a Murine Model of Spontaneous Prostate Cancer

Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3

B7-H3 expression in colorectal cancer: associations with clinicopathological parameters and patient outcome

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