Cancer Molecular Pathology, School of Medicine and Griffith Health Institute, Griffith Medical School, Griffith University, Gold Coast Campus, Gold Coast, Queensland 4222, Australia.
Department of Surgery, Gold Coast University Hospital, Gold Coast, Queensland, Australia.
Exp Cell Res. 2014 Aug 1;326(1):166-73. doi: 10.1016/j.yexcr.2014.06.013. Epub 2014 Jun 25.
The aims of the present study are to investigate the clinicopathological correlations of JK-1(FAM134B) expression and its relationship to carcinogenesis in a colorectal adenoma-adenocarcinoma model. JK-1(FAM134B) protein expression was studied in a colon cancer cell line by Western blot and immunocytochemistry. JK-1(FAM134B) expression profiles at mRNA and protein levels were investigated in cancer tissues from 236 patients with colorectal adenocarcinoma and 32 patients with colorectal adenoma using real-time polymerase chain reaction and immunohistochemistry. The findings were then correlated with the clinicopathological features of these tumours. JK-1(FAM134B) protein was demonstrated in the colon cancer cells by Western blot. The protein was located in the nuclei of the tumour cells at both cellular and tissue levels. In colorectal adenocarcinomas, lower levels of JK-1(FAM134B) protein expression were associated with younger age (p=0.032), larger tumour size (p=0.004), advanced cancer stages (p=0.016) and higher rates of cancer recurrence (p=0.04). Also, lower levels of JK-1(FAM134B) mRNA expression were associated with advanced cancer stages (p=0.02) and presence of lymphovascular invasion (p=0.014). Higher JK-1(FAM134B) mRNA and protein expression levels were identified in adenomas and non-neoplastic mucosae, compared to carcinomas (p=0.005). To conclude, JK-1(FAM134B) mRNA expression and JK1 (FAM134B) protein levels varied with the different stages of progression of colorectal tumours. The expression levels of the gene were associated with clinicopathological features in patients with colorectal adenocarcinoma suggesting that JK-1(FAM134B) gene has roles in controlling some steps in the development of the invasive phenotypes from colorectal adenoma to early staged as well as advanced staged colorectal adenocarcinomas.
本研究旨在探讨 JK-1(FAM134B)表达的临床病理相关性及其在结直肠腺瘤-腺癌模型中的致癌作用。通过 Western blot 和免疫细胞化学研究了结肠癌细胞系中 JK-1(FAM134B)蛋白的表达。使用实时聚合酶链反应和免疫组织化学技术,在 236 例结直肠腺癌和 32 例结直肠腺瘤患者的癌组织中研究了 JK-1(FAM134B)在 mRNA 和蛋白水平上的表达谱。然后将这些发现与这些肿瘤的临床病理特征相关联。通过 Western blot 在结肠癌细胞中证明了 JK-1(FAM134B)蛋白的存在。在细胞和组织水平上,蛋白定位于肿瘤细胞的核内。在结直肠腺癌中,JK-1(FAM134B)蛋白表达水平较低与年龄较轻(p=0.032)、肿瘤较大(p=0.004)、癌症分期较晚(p=0.016)和癌症复发率较高(p=0.04)有关。此外,JK-1(FAM134B)mRNA 表达水平较低与癌症分期较晚(p=0.02)和存在血管淋巴管侵犯(p=0.014)有关。与癌组织相比,腺瘤和非肿瘤黏膜中 JK-1(FAM134B)mRNA 和蛋白表达水平较高(p=0.005)。总之,JK-1(FAM134B)mRNA 表达和 JK1(FAM134B)蛋白水平随结直肠肿瘤进展的不同阶段而变化。该基因的表达水平与结直肠腺癌患者的临床病理特征相关,表明 JK-1(FAM134B)基因在控制从结直肠腺瘤到早期和晚期结直肠腺癌的侵袭表型的某些发展步骤中起作用。