The prognostic value of B7-H6 in esophageal squamous cell carcinoma

Zhou, Huan; Dong, Jun; Guo, Liyi; Wang, Xicheng; Wang, Kailin; Yang, Shu Yu

doi:10.1038/s41598-019-54731-9

Cited by 21 publications

(24 citation statements)

References 34 publications

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“…Among these signals, B7‐H6 /NKp30 pathway is involved in the NK cell‐mediated immune responses and tumor progression within a variety of tumors. Several previous studies demonstrated that the high expression of B7‐H6 was correlated with tumor progression and poor overall survival in some cancers (19–24, 27–29). Different research groups showed that B7‐H6 has no significant diagnostic or prognostic value in non‐small cell lung cancer and gastric cancer (26, 27).…”

Section: Discussionmentioning

confidence: 98%

“…B7‐H6 was also expressed in inflammatory monocytes, but not in healthy monocytes (18). Studies have reported that the expression of B7‐H6 is related to the metastasis of some cancers, and the B7‐H6 expression is negatively correlated with the overall survival (OS) rate of ovarian cancer, breast cancer, brain tumor, esophageal squamous cell carcinoma, cervical cancer, and esophageal squamous cell carcinoma (17, 19–24). However, the situation is not always the same, and it was found that the higher expression of B7‐H6 predicted favorable overall patient survival in gastric cancer (25).…”

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confidence: 99%

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Dual role of B7‐H6 as a novel prognostic marker in hepatocellular carcinoma

Qiu

Gao

Sun

et al. 2020

APMIS

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B7 homolog 6 (B7‐H6), a new member of the B7 family, is identified as an activating ligand for cytotoxicity triggering receptor 3 (NKp30) expressing on natural killer cells. The purpose of this study was to investigate the clinical significance of B7‐H6 in hepatocellular carcinoma (HCC). We evaluated B7‐H6 expression by immunohistochemistry in a cohort of 90 HCC tumors with clinical follow‐up, the potential relationship between the B7‐H6 expression and the clinicopathological characteristics of HCC patients was also analyzed. Stable B7‐H6 knockdown in hepatoma cell line was established to explore the function and mechanism of B7‐H6 in HCC. This study showed that high expression of B7‐H6 was significantly associated with smaller tumor size, single tumor number in HCC, but no significant association was found between B7‐H6 overexpression and other clinicopathological parameters. Moreover, Kaplan–Meier survival analysis showed that high expression of B7‐H6 was significantly correlated with better survival of HCC patients. Knockdown of B7‐H6 inhibited tumor cell proliferation and induced cell apoptosis. However, it also impaired the sensitivity of tumor cells to NK‐mediated lysis together with significantly decreased degranulation and IFN‐γ release of NK cells. These results indicated that B7‐H6 has a dual role in HCC. It could be an independent indicator for better survival of HCC and maybe a potential target for future cancer treatment.

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 99%

Dual role of B7‐H6 as a novel prognostic marker in hepatocellular carcinoma

Qiu

Gao

Sun

et al. 2020

APMIS

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“…While B7-H6 is usually not expressed in normal tissues, it is commonly found in different human cancers like small cell lung cancer [107], esophageal squamous cell carci-noma [108], gliomas [109], ovarian cancer [110] or HCC [106,111], where it is associated with poorer outcome. Unfortunately, no agents modulating B7-H6 signaling on tumor or NK cells are currently available [112].…”

Section: B7-h6mentioning

confidence: 99%

Immunmodulatory Treatment Strategies of Hepatocellular Carcinoma: From Checkpoint Inhibitors Now to an Integrated Approach in the Future

Ocker

Mayr

Kiesslich

et al. 2021

Cancers

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Background: Hepatocellular carcinoma (HCC) still represents a human tumor entity with very limited therapeutic options, especially for advanced stages. Here, immune checkpoint modulating drugs alone or in combination with local ablative techniques could open a new and attractive therapeutic “door” to improve outcome and response rate for patients with HCC. Methods: Published data on HCC experimental to pre-(clinical) treatment strategies from standard of care to novel immunomodulatory concepts were summarized and discussed in detail. Results: Overall, our knowledge of the role of immune checkpoints in HCC is dramatically increased in the last years. Experimental and pre-clinical findings could be translated to phase 1 and 2 clinical trials and became standard of care. Local ablative techniques of HCC could improve the effectivity of immune checkpoint inhibitors in situ. Conclusions: This review demonstrates the importance of immunomodulatory treatment strategies of HCC, whereby the “best treatment code” of immune checkpoint drugs, combination with ablative techniques and of timing must be evaluated in coming clinical trials.

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“…9 B7-H6 is upregulated and associated with poor prognosis (metastasis, worse overall survival) in a variety of solid tumors, including esophageal squamous cell, gastric, small lung, and breast cancers, among others. [10][11][12][13][14] However, little is known about its expression and role in tumorigenesis of hematological malignancies, such as acute myeloid leukemia (AML). One of the few studies being that of Chretien et al, who reported that B7-H6 is expressed on the cell surface of a very small number of leukemic blasts.…”

Section: Introductionmentioning

confidence: 99%

Bromodomain protein BRD4 is an epigenetic activator of B7-H6 expression in acute myeloid leukemia

et al. 2021

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B7-H6, a ligand for the NK activating receptor NKp30, has been identified as a biomarker of poor prognosis in several solid cancers. However, little is known about the role of B7-H6 and the mechanisms that control its expression in acute myeloid leukemia (AML). Epigenome modulation, including epigenomic reader dysregulation, is one of the hallmarks of AML. Bromodomain-containing protein 4 (BRD4), the best-known member of the BET family of epigenetic readers, is overexpressed in AML cells and regulates the transcription of genes involved in the pathogenesis of AML, as MYC oncogene. Here, we analyze the role of BRD4 in regulating B7-H6 in AML cells. Results demonstrated that the specific inhibition of BRD4 drastically reduces the expression of B7-H6 in AML cells. Histone acetylation mediated by CBP30/P300 facilitates the binding of BRD4 to the B7-H6 promoter, which recruits the P -TEFb elongation factor that phosphorylates RNA polymerase II, thereby activating B7-H6 transcription. BRD4 also co-bounded with JMJD6 at the distal enhancer of the B7-H6 gene. Metabolic modulation with metformin modifies the acetylation pattern in the B7-H6 promoter, impairing BRD4 binding, thereby inhibiting B7-H6 expression. B7-H6 knockdown induces the apoptosis in HEL-R cell line. Moreover, a high level of B7-H6 expression in AML patients is related to increased BRD4 levels, myelodysplastic-derived AML, and del5q, the two latter being associated with poor prognosis. Our data show that BRD4 is a positive regulator of the pro-tumorigenic molecule B7-H6 and that the blockage of the B7-H6 is a potential therapeutic target for the treatment of AML.

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The prognostic value of B7-H6 in esophageal squamous cell carcinoma

Cited by 21 publications

References 34 publications

Dual role of B7‐H6 as a novel prognostic marker in hepatocellular carcinoma

Dual role of B7‐H6 as a novel prognostic marker in hepatocellular carcinoma

Immunmodulatory Treatment Strategies of Hepatocellular Carcinoma: From Checkpoint Inhibitors Now to an Integrated Approach in the Future

Bromodomain protein BRD4 is an epigenetic activator of B7-H6 expression in acute myeloid leukemia

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