| 卢 文,唐丽萍,胡晓君,刘 倩,邵嘉艺,李晓梅,马敬全.共刺激分子B7-H4在宫颈癌中的表达及意义[J].,2017,17(13):2426-2430 |
| 共刺激分子B7-H4在宫颈癌中的表达及意义 |
| Expression of Costimulatory Molecule B7-H4 and Its Significance in Cervical Carcinoma |
| 投稿时间：2016-05-23 修订日期：2016-06-18 |
| DOI：10.13241/j.cnki.pmb.2017.13.007 |
| 中文关键词: B7-H4 Fas Caspase-3裂解片段 宫颈癌 免疫逃逸 |
| 英文关键词: B7-H4 Fas Caspase-3 cleavage Cervical cancer Immune Escape |
| 基金项目:黑龙江省自然科学基金项目(D201136)；黑龙江省博士后科学研究基金项目（LBH-Z06252） |
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| 中文摘要: |
| 摘要 目的：肿瘤微环境中免疫共刺激分子B7-H4与其配体结合后可提供免疫抑制信号，调控肿瘤组织中的免疫应答。本研究探讨B7-H4、Fas及Caspase-3裂解片段在宫颈鳞状细胞癌中的表达及其与临床病理因素的关系，分析其参与肿瘤免疫逃逸的机制。方法：应用免疫组织化学SP法检测23例正常宫颈上皮、38例宫颈上皮内瘤变(CIN)和132例宫颈鳞状细胞癌组织中B7-H4、Fas及Caspase-3裂解片段的表达水平，分析其与宫颈癌各临床病理因素的相关性。结果：B7-H4在正常宫颈上皮组织中不表达，在CIN组织中微弱表达，在宫颈鳞状细胞癌组织中高表达。B7-H4表达与肿瘤的临床分期、淋巴结转移、原发肿瘤大小和肿瘤浸润深度有关，B7-H4与Fas蛋白表达呈现负相关，与Caspase-3裂解片段存在共表达关系。结论：B7-H4在宫颈鳞状细胞癌中过表达可引起Fas蛋白表达下调和Caspase-3裂解片段增多，抑制肿瘤细胞发生凋亡，参与肿瘤逃避宿主的免疫监视，从而促发宫颈癌的发生和发展。阻断B7-H4通路途径，有望成为宫颈鳞状细胞癌治疗的新靶点。 |
| 英文摘要: |
| ABSTRACT Objective: Immune costimulatory molecules B7-H4 binds with its ligand in the tumor micro-environment, which pro- vides immune inhibitory signals, and further controls the immune response in tumor tissues. In this paper, we examined the expressions of B7-H4, Fas and Caspase-3 cleavage in cervical squamous cell carcinoma and tried to figure out their connections with it's clinical patho- logical factors to obtain the mechanism of tumor cell immune escape. Methods: Immunohistochemical method (SP) was applied to detect the expression levels of B7-H4, Fas and Caspase-3 cleavage in 23 normal cases of nomal cervical epithelium, 38 cases of cervical intraep- ithelial neoplasia (CIN) and 132 cases of cervical squamous cancer cells, then analyzed its correlation with the clinicopathological factors in cervical cancer. Results: B7-H4 sshowed no expression in normal cervical epithelial tissues, showed weak expression in CIN tissues and high expression in cervical squamous cell carcinoma; B7-H4 expression was directly related to the clinical stage, lymph node metas- tasis, primary tumor size and depth of tumor invasion. B7-H4 showed negative correlation with the expression of Fas protein, and shared a co-expression with Caspase-3 cleavage. Conclusion: B7-H4 showing excessive expressions in cervical squamous cell carcinoma will lead to down-regulations of Fas protein expression and increasements of Caspase-3 cleavage. All these worked together induced tumor evading of host immune surveillance, thus inhibiting the apoptosis of tumor cells, which promotes the occurrence and deterioration of cervical cancer. Blocking the B7-H4 pathway is expected to become a new target in the treatment of cervical squamous cell carcinoma. |
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