Department of Clinical Laboratory, Maternity and Child-Care Hospital of Pingshan District (Maternity and Child-Care Hospital, Shenzhen University), Shenzhen, Guangdong, China.
Eur Rev Med Pharmacol Sci. 2019 Aug;23(16):6878-6887. doi: 10.26355/eurrev_201908_18727.
Renal carcinoma is the second most common cancer in the urinary system with an increasing trend. The major treatment for renal carcinoma is surgery, which results in unfavorable prognosis at times. As a tissue-specific marker for tumor, microRNA (miR) exerts its functions via facilitating oncogenic gene expression or suppressing tumor suppressor gene. MiR-184 is known to be abnormally expressed in various tumors. There are few studies about the lack of miR-184 expression in renal carcinoma.
Real time-Polymerase Chain Reaction (PCR) was used to measure the expression of miR-184 in 38 renal carcinoma and adjacent tissues. The in vitro cultured renal carcinoma cell line ACHN was transfected with miR-184 mimic or inhibitor. The expression of miR-184 was measured by real time-PCR, and the cell proliferation was measured by MTT assay. The cell colony formation was examined, and the cell invasion potency was assessed by transwell assay. The apoptotic activity was measured by flow cytometry, and the Western blot detected protein expression change of β-catenin/TCF3 pathway.
Compared to tumor-adjacent tissues, miR-184 and β-catenin/TCF3 showed an elevated expression in renal carcinoma tissues which were further increased with elevated RC stages (p<0.05). The transfection of miR-184 mimic into ACHN cells increased its expression, enhanced ACHN cell proliferation, colony formation, inhibited apoptosis, promoted tumor cell invasion, and increased the expression of β-catenin and TCF4 proteins (p<0.05 compared to NC control group).
MiR-184 is up-regulated in renal carcinoma tissues. The downregulation of miR-184 in renal carcinoma cells could facilitate cell apoptosis and inhibited tumor proliferation or invasion possibly via modulating β-catenin/TCF4 pathway.
肾细胞癌是泌尿系统中第二常见的癌症，且呈上升趋势。肾细胞癌的主要治疗方法是手术，但有时预后不佳。微小 RNA（miRNA）作为一种组织特异性肿瘤标志物，通过促进致癌基因表达或抑制肿瘤抑制基因发挥作用。miR-184 在各种肿瘤中表达异常。关于肾细胞癌中 miR-184 表达缺失的研究较少。
实时聚合酶链反应（PCR）用于测量 38 例肾细胞癌及相邻组织中 miR-184 的表达。将 miR-184 模拟物或抑制剂转染至体外培养的肾癌细胞系 ACHN 中。通过实时 PCR 测量 miR-184 的表达，通过 MTT 测定法测量细胞增殖。通过集落形成实验检测细胞集落形成，通过 Transwell 测定法评估细胞侵袭能力。通过流式细胞术测量细胞凋亡活性，Western blot 检测 β-catenin/TCF3 通路蛋白表达变化。
与肿瘤相邻组织相比，miR-184 和 β-catenin/TCF3 在肾细胞癌组织中表达升高，且随着 RC 分期的升高而进一步升高（p<0.05）。将 miR-184 模拟物转染至 ACHN 细胞中可增加其表达，增强 ACHN 细胞增殖、集落形成，抑制细胞凋亡，促进肿瘤细胞侵袭，并增加 β-catenin 和 TCF4 蛋白的表达（与 NC 对照组相比，p<0.05）。
miR-184 在肾细胞癌组织中上调。下调肾癌细胞中的 miR-184 可能通过调节β-catenin/TCF4 通路促进细胞凋亡并抑制肿瘤增殖或侵袭。
