Department of Pathology and Molecular Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Department of Gastroenterological Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
J Pathol Clin Res. 2023 Sep;9(5):354-366. doi: 10.1002/cjp2.326. Epub 2023 May 28.
Diabetes mellitus (DM) is a risk factor for pancreatic ductal adenocarcinoma (PDAC) that promotes the promoter methylation of CDH1. It is still unclear whether DM can exert other epigenetic effects, such as altering microRNA (miR) expression, in PDAC. The expression of miR-100-5p is known to be changed in DM patients and can suppress the expression of E-cadherin. In this study, the correlation between DM status and dual epigenetic changes was evaluated in PDAC specimens from patients who underwent radical surgical resection. A total of 132 consecutive patients with PDAC were clinicopathologically evaluated. E-cadherin and nuclear β-catenin expression was measured using immunohistochemistry. DNA and miRs were extracted from the main tumor site on formalin-fixed paraffin-embedded tissue sections. TaqMan miR assays were applied to assess miR-100-5p expression. Bisulfite modification was conducted on the extracted DNA, which was then subjected to methylation-specific polymerase chain reaction. Immunohistochemistry revealed that decreased E-cadherin expression and increased nuclear β-catenin expression were significantly associated with DM and poor tumor cell differentiation. The presence of long-duration DM (≥3 years) was a significant factor contributing to CDH1 promoter methylation (p < 0.01), while miR-100-5p expression was proportionally correlated with the preoperative HbA1c level (R = 0.34, p < 0.01), but not the duration of DM. The subjects with high miR-100-5p expression and CDH1 promoter methylation showed the highest level of vessel invasion and prevalence of tumor size ≥30 mm. PDAC subjects with dual epigenetic changes showed poorer overall survival (OS) than those with a single epigenetic change. miR-100-5p expression ≥4.13 and CDH1 promoter methylation independently predicted poor OS and disease-free survival (DFS) in the multivariate analysis. OS and DFS worsened in DM subjects with both HbA1c ≥ 6.5% and DM duration ≥3 years. Thus, DM is associated with two modes of epigenetic change by independent mechanisms and worsens prognosis.
糖尿病(DM)是胰腺导管腺癌(PDAC)的一个危险因素,可促进 CDH1 的启动子甲基化。目前尚不清楚 DM 是否可以在 PDAC 中发挥其他表观遗传效应,例如改变 microRNA(miR)的表达。miR-100-5p 的表达在 DM 患者中已知发生改变,并且可以抑制 E-钙黏蛋白的表达。在这项研究中,评估了接受根治性手术切除的 PDAC 标本中 DM 状态与双重表观遗传变化的相关性。对 132 例连续 PDAC 患者进行了临床病理评估。使用免疫组织化学法测量 E-钙黏蛋白和核 β-连环蛋白的表达。从福尔马林固定石蜡包埋组织切片的主要肿瘤部位提取 DNA 和 miRs。应用 TaqMan miR 检测法评估 miR-100-5p 的表达。对提取的 DNA 进行亚硫酸氢盐修饰,然后进行甲基化特异性聚合酶链反应。免疫组织化学显示,E-钙黏蛋白表达降低和核 β-连环蛋白表达增加与 DM 和肿瘤细胞分化不良显著相关。长期 DM(≥3 年)的存在是 CDH1 启动子甲基化的重要因素(p<0.01),而 miR-100-5p 的表达与术前 HbA1c 水平呈比例相关(R=0.34,p<0.01),但与 DM 的持续时间无关。miR-100-5p 表达较高且 CDH1 启动子甲基化的患者表现出最高的血管侵犯程度和肿瘤大小≥30mm 的发生率。具有双重表观遗传变化的 PDAC 患者的总生存(OS)较具有单一表观遗传变化的患者差。miR-100-5p 表达≥4.13 和 CDH1 启动子甲基化在多变量分析中独立预测了不良 OS 和无病生存(DFS)。HbA1c≥6.5%且 DM 持续时间≥3 年的 DM 患者的 OS 和 DFS 恶化。因此,DM 通过独立机制与两种表观遗传改变模式相关,并使预后恶化。