Dong Xiancheng, Lv Bin, Li Yusong, Cheng Qinghua, Su Chuan, Yin Guoyong
Nanjing Medical University, Nanjing, PR China; Department of Orthopedics, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, PR China.
Nanjing Medical University, Nanjing, PR China.
Arch Biochem Biophys. 2017 Sep 15;630:47-53. doi: 10.1016/j.abb.2017.07.011. Epub 2017 Jul 20.
Accumulating documents have been suggested that microRNA-143 (miR-143) function as a tumor suppressor, involved in many biological processes including tumor initiation and progression. However, the biological function and molecular mechanism of miR-143 in Osteosarcoma (OS) still remains to be further investigated. Despite many efforts have been made, the prognosis of OS is still unsatisfied. Thus, exploring the underlying mechanism of OS and finding new treatment targets is essential for improving the survival rate of OS patients. In our study, we determined the level of miR-143 in clinical OS tissues and cells, and explored its function and underlying mechanisms in the tumorigenesis of OS. Our findings revealed that miR-143 expression was significantly downregulated in OS tissues and cell lines. Gain-of-function assays indicated that forced expression of miR-143 in OS cells inhibited cell proliferation and migration/invasion. Bioinformatics and luciferase reporter assays confirmed that MAPK7 was targets gene of miR-143. The results of the present study indicated that miR-143 could be a potential target for treating OS.
越来越多的文献表明，微小RNA-143（miR-143）作为一种肿瘤抑制因子，参与包括肿瘤发生和进展在内的许多生物学过程。然而，miR-143在骨肉瘤（OS）中的生物学功能和分子机制仍有待进一步研究。尽管已经做出了许多努力，但骨肉瘤的预后仍然不尽人意。因此，探索骨肉瘤的潜在机制并寻找新的治疗靶点对于提高骨肉瘤患者的生存率至关重要。在我们的研究中，我们测定了临床骨肉瘤组织和细胞中miR-143的水平，并探讨了其在骨肉瘤发生中的功能和潜在机制。我们的研究结果显示，miR-143在骨肉瘤组织和细胞系中的表达明显下调。功能获得实验表明，在骨肉瘤细胞中强制表达miR-143可抑制细胞增殖和迁移/侵袭。生物信息学和荧光素酶报告基因实验证实，丝裂原活化蛋白激酶7（MAPK7）是miR-143的靶基因。本研究结果表明，miR-143可能是治疗骨肉瘤的一个潜在靶点。
