Chen Jingyao, Xia Di, Xu Muming, Su Ruibing, Lin Wenting, Guo Dan, Chen Guangcan, Liu Shuhui
Department of Pathology, Shantou University Medical College, Shantou, China.
Department of Abdominal Surgery, The Tumor Hospital of Shantou University Medical College, Shantou, China.
Front Oncol. 2020 May 14;10:559. doi: 10.3389/fonc.2020.00559. eCollection 2020.
Gastric cardia cancer (GCC) arises in the area of the stomach adjoining the esophageal-gastric junction and has unique risk factors. It was suggested that the involvement of is associated with GCC from high-risk population. Myeloid differentiation factor 88 (MyD88) is a crucial adaptor molecule in Toll-like signaling pathway recognizing . Its role in GCC has not been elucidated yet. In this study, our purpose is to investigate the expression and significance of MyD88 in GCC tissue. Expression of MyD88 and nuclear factor κB (NF-κB) p105/p50 and infection of were detected by immunohistochemistry in gastric cardia tissue. The correlation of MyD88 expression to NF-κB p105/p50 expression, infection, and clinicopathologic characteristics in gastric cardia tissue was analyzed. The involvement of MyD88 in patient prognosis was also analyzed. Our data showed that the expression of MyD88 elevated from normal mucosa to inflammation ( = 0.071). The expression of MyD88 was enhanced in GCC tissues by contrast to non-malignant cardia mucosa ( = 0.025). What's more, overexpression of MyD88 was detected in intestinal-type adenocarcinoma with inflammation. Patients with high MyD88 staining revealed a better differentiation ( = 0.02). MyD88 also positively correlated with NF-κB p105/p50 expression ( = 0.012) in cancer tissue. Expression of MyD88 was increased but not significantly in biopsies with infection compared with non-infected biopsies. Multivariate analyses revealed lymph node metastasis but not MyD88 expression was an independent predictor for patient survival. These findings provide pathological evidence that upregulating MyD88 and inducing inflammation might be involved in gastric cardia carcinogenesis in high-risk population. MyD88 plays a role in gastric cardia carcinogenesis with NF-κB pathway activation. Higher MyD88 expression is not a major prognostic determinant in GCC, but it may relate to the tumor cell differentiation.
贲门癌（GCC）起源于胃与食管-胃交界相邻的区域，且具有独特的危险因素。有研究表明，[此处原文缺失相关内容]的参与与高危人群的贲门癌有关。髓样分化因子88（MyD88）是Toll样信号通路中识别[此处原文缺失相关内容]的关键衔接分子。其在贲门癌中的作用尚未阐明。在本研究中，我们的目的是探讨MyD88在贲门癌组织中的表达及意义。通过免疫组织化学检测贲门组织中MyD88、核因子κB（NF-κB）p105/p50的表达以及[此处原文缺失相关内容]的感染情况。分析MyD88表达与NF-κB p105/p50表达、[此处原文缺失相关内容]感染以及贲门组织临床病理特征之间的相关性。同时分析MyD88对患者预后的影响。我们的数据显示，MyD88的表达从正常黏膜到炎症组织呈升高趋势（P = 0.071）。与非恶性贲门黏膜相比，MyD88在贲门癌组织中的表达增强（P = 0.025）。此外，在伴有炎症的肠型腺癌中检测到MyD88过表达。MyD88染色高的患者显示出更好的分化程度（P = 0.02）。在癌组织中，MyD88也与NF-κB p105/p50表达呈正相关（P = 0.012）。与未感染活检组织相比，[此处原文缺失相关内容]感染的活检组织中MyD88表达增加，但差异不显著。多因素分析显示，淋巴结转移而非MyD88表达是患者生存的独立预测因素。这些发现提供了病理学证据，即上调MyD88并诱导炎症可能参与高危人群贲门癌的发生。MyD88通过激活NF-κB途径在贲门癌发生中发挥作用。较高的MyD88表达不是贲门癌的主要预后决定因素，但可能与肿瘤细胞分化有关。
