Fındık Damla Gül, Şahin Erhan, Türelik Özlem, Güneri Gürkan
Department of Histology and Embryology, Faculty of Medicine, Bilecik Şeyh Edebali University, Bilecik, Turkey.
Department of Pathology, Faculty of Medicine, Bilecik Şeyh Edebali University, Bilecik, Turkey.
Biomol Biomed. 2024 Dec 11;25(1):62-70. doi: 10.17305/bb.2024.10981.
Colorectal cancer poses a significant global health challenge, with a considerable proportion arising from colon adenomas. Understanding the molecules involved in the carcinogenesis process is crucial for improving colon cancer diagnosis and prognosis. While research on the role of epiplakin in cancer remains limited compared to other plakin group proteins, comprehending its expression patterns and correlations can offer valuable insights into colon carcinogenesis. In this study, we analyzed 60 tissue samples, including colon adenocarcinomas, tubular adenomas (low malignancy risk group), tubulovillous adenomas (high malignancy risk group), and adjacent normal colon tissues. Classification and grading were reevaluated by histological examination. Immunohistochemistry was performed to assess epiplakin and Ki67 expression. Epiplakin optical density and the Ki67 proliferation index were calculated using ImageJ. Statistical analyses were conducted to evaluate correlations and significance. Epiplakin expression was significantly decreased in colon adenocarcinomas [optical density median 4.04 (95% CI, 3.98 to 4.24)] and tubulovillous adenomas [4.32 (95% CI, 4.08 to 4.32)] compared to normal colon tissues [4.61 (95% CI, 4.50 to 4.67)] and tubular adenomas [4.87 (95% CI, 4.67 to 4.88)] (P < 0.05). Moreover, adenoma groups exhibited higher proliferation indices (P < 0.05), and a positive correlation was found between epiplakin expression and the Ki67 proliferation index (r = 0.317, P < 0.05). Our study highlights the potential significance of epiplakin in colorectal cancer. Decreased epiplakin expression is associated with colon malignancy progression, suggesting its role as a potential marker.
结直肠癌是一项重大的全球健康挑战,其中相当一部分源于结肠腺瘤。了解致癌过程中涉及的分子对于改善结肠癌的诊断和预后至关重要。虽然与其他斑块蛋白家族蛋白相比,关于表皮斑蛋白在癌症中作用的研究仍然有限,但了解其表达模式和相关性可为结肠致癌作用提供有价值的见解。在本研究中,我们分析了60个组织样本,包括结肠腺癌、管状腺瘤(低恶性风险组)、绒毛状管状腺瘤(高恶性风险组)以及相邻的正常结肠组织。通过组织学检查重新评估分类和分级。进行免疫组织化学以评估表皮斑蛋白和Ki67的表达。使用ImageJ计算表皮斑蛋白光密度和Ki67增殖指数。进行统计分析以评估相关性和显著性。与正常结肠组织[4.61(95%置信区间,4.50至4.67)]和管状腺瘤[4.87(95%置信区间,4.67至4.88)]相比,结肠腺癌[光密度中位数4.04(95%置信区间,3.98至4.24)]和绒毛状管状腺瘤[4.32(95%置信区间,4.08至4.32)]中表皮斑蛋白表达显著降低(P<0.05)。此外,腺瘤组表现出更高的增殖指数(P<0.05),并且发现表皮斑蛋白表达与Ki67增殖指数之间存在正相关(r = 0.317,P<0.05)。我们的研究突出了表皮斑蛋白在结直肠癌中的潜在重要性。表皮斑蛋白表达降低与结肠恶性进展相关,表明其作为潜在标志物的作用。