Abstract
B7-H6, a new member of B7-family ligand, also known as NCR3LG1, plays an important role in NK cells mediated immune responses. Many studies have shown that it is highly expressed in various human cancers, and its expression levels are significantly associated with cancer patients’ clinicopathological parameters and postoperative prognoses. But, still the exact role of B7-H6 expression in human glioma remains elusive. In the present study, we have characterized the B7-H6 expression in the human glioma tissues as well as glioma cell lines, U87 and U251. We observed that B7-H6 was highly expressed in the human glioma tissues, and its expression was significantly associated with cancer progression. By using the RNA interference technology, we successfully ablated B7-H6 expression in human glioma cell lines to further study its contribution towards various biological features of this malignancy. Our study identified that the B7-H6 knockdown in U87 and U251 glioma cells significantly suppressed cell proliferation, migration, invasion, and enhanced apoptosis along with induction of cell cycle arrest. It thus suggested that B7-H6 play an important role in the regulation of the biological behavior of these glioma cells. However, the detailed mechanism of B7-H6 mediated regulation of glioma cancer cell transformation and its prognostic value merits further investigation.
Highlights
Glioma, the most common tumor of the central nervous system, accounts for about 40–50% of the human adult brain tumors [1]
We observed that B7-H6 was highly expressed in the human glioma tissues, and its expression was significantly associated with cancer progression
Our study identified that the B7-H6 knockdown in U87 and U251 glioma cells significantly suppressed cell proliferation, migration, invasion, and enhanced apoptosis along with induction of cell cycle arrest
Summary
The most common tumor of the central nervous system, accounts for about 40–50% of the human adult brain tumors [1]. The patients with malignant glioma usually have a poor prognosis and a high rate of mortality [2]. Despite the availability of multiple strategies such as novel surgical treatments and effective radiation/chemotherapy for the diagnosis of high-grade glioma in recent decades, the overall 5-year survival rate of the patients still remains poor. The NK cells regulate both innate and adaptive immune responses via secreting pro-inflammatory cytokines and chemokines, mediating cytotoxic activity through direct lysis of the target cells [4]. These cell express activating receptors on their surface such as NKp30, NKp44 and NKp46, which contribute essentially in the recognition and elimination of abnormal target cells [5]. Cancer cells escape NKcell-mediated recognition in tumor microenvironment via expressing certain ligands like PD-L1 and so on [6, 7]
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