期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 234, 期 9, 页码 15025-15034出版社
WILEY
DOI: 10.1002/jcp.28142
关键词
HMGB1; miRNA-505; proliferation; renal cell carcinoma
microRNAs have been recognized to regulate a wide range of biology of renal cell carcinoma (RCC). Although miR-505 has been reported to play as a suppressor in several human tumors, the physiological function of miR-505 in RCC still remain unknown. Therefore, the role of miR-505 and relevant regulatory mechanisms were investigated in RCC in this study. Quantitative real-time polymerase chain reaction was conducted to detect the expression of miR-505 and high mobility group box 1 (HMGB1) in both RCC tissues and cell lines. Immunohistochemical staining was used to assess the correlation between HMGB1 expression and PCNA expression in RCC tissues. Subsequently, the effects of miR-505 on proliferation were determined in vitro using cell counting kit-8 proliferation assays and 5-ethynyl-2-deoxyuridine incorporation. The molecular mechanism underlying the relevance between miR-505 and HMGB1 was confirmed by luciferase assay. Xenograft tumor formation was used to reflect the proliferative capacity of miR-505 in vivo experiments. Overall, a relatively lower miR-505 and higher HMGB1 expression in RCC specimens and cell lines were found. HMGB1 was verified as a direct target of miR-505 by luciferase assay. In vitro, overexpression of miR-505 negatively regulates HMGB1 to suppress the proliferation in Caki-1; meanwhile, knock-down of miR-505 negatively regulates HMGB1 to promote the proliferation in 769P. In addition, in vivo overexpression of miR-505 could inhibit tumor cell proliferation in RCC by xenograft tumor formation. Therefore, miR-505, as a tumor suppressor, negatively regulated HMGB1 to suppress the proliferation in RCC, and might serve as a novel therapeutic target for RCC clinical treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据