B7 homolog 6 promotes the progression of cervical cancer

Guo, Ruimeng; Liu, Guoyan; Li, Changying; Liu, Xuejing; Xu, Yanying; Yang, Weina; Wang, Fang

doi:10.3892/etm.2021.10206

Cited by 4 publications

(10 citation statements)

References 29 publications

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“…Interestingly, however, some studies [25,26] have obtained opposite results, suggesting that B7-H6 can lead to immune escape of tumor cells through speci c binding with NKp30, thus avoiding the protective barrier of the body's rst immune defense line. We study found that since the onset of cervical intraepithelial neoplasia, the expression of B7-H6 began to appear in cervical lesion tissues [9]. Therefore, it is speculated that B7-H6 not only plays role in the progression of cervical disease, but also mediates the body's innate immunity to participate in the immune regulation of cervical lesion through its special association with NKp30.…”

Section: Discussionmentioning

confidence: 79%

“…B7-H6 is a member of the B7 family. Our previous study found that B7-H6 expressed on the cervical cancer is expected to become a new biological therapeutic target for cervical cancer [9]. Interestingly, however, B7-H6, also known as NK cytotoxic receptor 3 ligand 1, can bind speci cally to the surface active receptor NKp30 of NK cells through signaling motifs [13][14].…”

Section: Discussionmentioning

confidence: 99%

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B7-H6 promotes the killing activity of NK cells against cervical cancer through the downstream ERK pathway of NKp30

Guo

Chai²,

et al. 2023

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OBJECTIVE As a ligand of NKp30, B7 homolog 6 (B7-H6) is involved in the immune regulation of various tumors. The aim of this study was to clarify the effect of B7-H6 expressed in HeLa cells on NK cell killing function. METHODS The expression of B7H6 was changed in HeLa cells using short hairpin RNA. Furthermore the effect of B7-H6 on the killing function of NK cell was analyzed after cell co-culture. Flow cytometry was used to detect NKp30 expression, degranulation function, perforin (PFP) and Granzyme B (GZMB) secretion function of NK cells. Enzyme-linked immunosorbent assay (ELISA) was used to detect interferon-γ (INF-γ) production function. The cytotoxicity of NK-92 cells was determined using the CytoTox 96 Non-Radio active Cytotoxicity Assay. Western blotting (WB) detection was used to detect the ERK phosphorylation level in NK cells. RESULTS When NK-92 cells co-cultivated with HeLa cells with different expression levels of B7-H6, the expression of NKp30, NK-92 cell killing rate, PFP and INF-γ production, and degranulation function were correspondingly changed in NK cells, but there is no effcet on GZMB production. After cell co-culture, ERK phosphorylation level in NK cells was increased gradually with the up-regulation of B7-H6 expression. CONCLUSIONS B7-H6 can enhance the killing function of NK cells to HeLa cells by activating the NKp30 downstream ERK signaling pathway.

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

B7-H6 promotes the killing activity of NK cells against cervical cancer through the downstream ERK pathway of NKp30

Guo

Chai²,

et al. 2023

Preprint

Self Cite

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“…Recent evidence has shown that cancer stemness was negatively associated with antitumor immunity [36,44]. In the current work, we investigated the cancer stemness feature in examined groups.…”

Section: Discussionmentioning

confidence: 99%

B7H6 silencing increases chemosensitivity to dacarbazine and suppresses cell survival and migration in cutaneous melanoma

et al. 2023

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Cutaneous melanoma (CM) is a highly metastatic cancer whose incidence rate is heightening worldwide. B7H6, as one of the co-stimulatory ligands of the B7 family, is expressed in malignant cells, involved in tumorigenesis. This study aimed to investigate the significance of B7H6 in CM cell chemosensitivity and metastatic ability. A375 CM cells were transfected with B7H6-siRNA and treated with dacarbazine individually or combined. The MTT assay to estimate half-maximal inhibitory concentration of dacarbazine and cell viability, the apoptotic induction using Annexin V/PI, cell cycle progression via flow cytometry, and wound healing assay for determining the migration ability of cells and assessing the clonogenic potential of A375 cells were executed. Functional analyses were performed to evaluate changes in A375 cells. The results illustrated that B7H6 suppression significantly increased the chemosensitivity of A375 cells to dacarbazine. Apoptosis induction by dacarbazine was enhanced after B7H6 knockdown through modulating Caspase-3, Bax, and Bcl-2 mRNA levels. Western blotting indicated enhancement of cleaved caspase-3 protein expression in treatment groups. A375 cells were arrested at the sub-G1 and S phases when using B7H6-siRNA and dacarbazine. B7H6 suppression combined with dacarbazine restrained cell migration through suppression of matrix metalloproteinase (MMP) expression, including MMP2, MMP3, and MMP9. In addition, the clonogenic ability of A375 cells was decreased by downregulating Sox2, Nanog, and CD44 mRNA levels. A visible decrement in STAT3 protein expression was observed in the combination group. Hence, our findings revealed that B7H6 knockdown with dacarbazine could be a promising treatment approach for cutaneous melanoma.

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“…The recently studied B7 homolog 6 (B7-H6) protein is a tumour biomarker that is upregulated in cervical precancer and cancer, where the biomarker's expression correlates with disease progression. B7-H6's stage-dependent expression suggests its possible utility for predicting prognosis [109].…”

Section: Cervical Cancermentioning

confidence: 99%

“…B7-H6's stage-dependent expression suggests its possible utility for predicting prognosis. 109 Other protein biomarkers include osteopontin (OPN), 110 protein cyclin-dependent kinase inhibitor (p16), and topoisomerase II-alpha (TOP2A). 111 OPN was observed to be upregulated in cervical cancer, 110 while p16 and TOP2A overexpression were related to precancer and cancer.…”

Section: Cervical Cancermentioning

confidence: 99%