B7-H6 expression is induced by lipopolysaccharide and facilitates cancer invasion and metastasis in human gliomas

Expression of B7-H6 expression in human hepatocellular carcinoma and its clinical significance

“…Jiang et al have also shown that the knockdown of B7-H6 expression in U87 and U251 glioma cells significantly suppresses cell proliferation, migration and invasion, leading to enhanced apoptosis along with the induction of cell cycle arrest [5]. Moreover, Che et al also confirmed the contribution of B7-H6 in cellular function regulation of human glioma cells, and moreover, they also showed that, the knockdown of B7-H6 could also induce the increased expression levels of E-cadherin and Bcl-2 associated X protein, and the decreased expression levels of vimentin, N-cadherin, MMP-2, MMP-9 and survivin, which further supported that B7-H6 was involved in the promotion of cancer progression [23]. Wu et al have also demonstrated that B7-H6 is widely expressed in B-cell lymphomas and that the knockdown of B7-H6 expression can not only inhibit the proliferation, colony formation, migration and invasion of lymphoma cells but can also increase cell apoptosis and sensitivity to vincristine and dexamethasone [24].…”

Positive staining of the immunoligand B7-H6 in abnormal/transformed keratinocytes consistently accompanies the progression of cervical cancer

“…These reports include evidence of B7-H6 in the following pathological conditions: ovarian carcinoma, oral squamous carcinoma, non-Hodgkin lymphoma, astrocytoma, glioma, melanoma, atopic dermatitis, and liver tissue from patients with hepatitis B virus-related acute-on-chronic liver failure, among others. Interestingly, the severity of these diseases has been positively correlated with the presence of B7-H6; in some cases, a negative correlation between B7-H6 expression and overall survival has also been seen, as well as a positive correlation between disease progression and B7-H6 [9,11,15,[19][20][21][22][23]]. In contrast, in some pathologies, such as in non-small cell lung cancer or gastric carcinoma, B7-H6 has shown limited value as a prognostic marker for the disease [24,25].…”

“…Under inflammatory conditions, it has been proposed that both forms (membrane and soluble) of B7-H6 could be regulated by different mechanisms including TRIF or Myd88-dependent TLR signaling pathways [9,17]. Therefore, considering that cervical microbiota changes through progressive intraepithelial lesions advancing toward cancer, which is characterized by the presence of gram-negative bacteria, including Fusobacterium spp [31], we cannot discard the possibility that microbial diversity associated with either squamous cervical carcinoma or cervical adenocarcinoma might be able to activate different inflammatory pathways influencing consequently the production of soluble or membrane forms of B7-H6.…”

“…The identification of NKp30 ligands has been a great challenge, and to date little is known about this topic. However, in the last decade, the molecule B7-H6 has been revealed as a novel NKp30 endogenous immunoligand expressed in a variety of tumors and stressed cells, but not expressed in healthy tissues [9][10][11][12][13][14].…”

“…Due to the fact that B7-H6 belongs to a family composed of both co-stimulatory and co-inhibitory receptors [14], it follows that the supposition has arisen that this ligand for NKp30 also may play a role in the biology of the tumor cells themselves, perhaps promoting tumor cell survival, proliferation, migration and invasion [9,15,16]. Cell culture studies have shown that the interaction between NKp30/B7-H6 drives a signaling cascade in the NK cell that culminates in degranulation and IFN-γ secretion [14].…”