MiR-429 suppresses the progression and metastasis of osteosarcoma by targeting ZEB1

نویسندگان

  • Yi Deng
  • Fujun Luan
  • Li Zeng
  • Yanjun Zhang
  • Kunlong Ma
چکیده

MiR-429 functions as a tumor suppressor and has been observed in multiple types of cancer, but the effects and mechanisms of miR-429 in osteosarcoma are poorly understood. This study is performed to evaluate the functions of miR-429 in the progression of osteosarcoma. Firstly, the miR-429 expression in osteosarcoma tissues and osteosarcoma cells was detected using real time PCR, and the relationship between miR-429 expression and overall survival of osteosarcoma was analyzed. Secondly, the effects of miR-429 on the migration, invasion, proliferation and apoptosis of osteosarcoma cells were evaluated using transwell assay, wound-healing assay, CCK-8 assay and flow cytometry, respectively. Proteins related to epithelial-mesenchymal transition (EMT), E-cadherin, Vimentin, N-cadherin and Snail, were also detected using Western blot. Finally, the target gene of miR-429 in osteosarcoma was predicted and verified using dual luciferase assay and the expression correlation between them was analyzed using Pearson's correlation. MiR-429 was down-regulated in osteosarcoma tissues and osteosarcoma cells; the expression level of miR-429 was associated with the prognosis of osteosarcoma. High level of miR-429 in osteosarcoma cells significantly suppressed the migration, invasion and proliferation of cells but induced cells apoptosis. Furthermore, high level of miR-429 in osteosarcoma cells obviously increased the expression of E-cadherin protein but decreased the expression of Vimentin, N-Cadherin and Snail proteins. EMT inducer ZEB1 was the target gene of miR-429 and the expression of ZEB1 was negatively related to the miR-429 expression in osteosarcoma. In conclusion, miR-429 may functions as a tumor suppressor and be down-regulated in osteosarcoma. MiR-429 may suppress the progression and metastasis of osteosarcoma by down-regulating the ZEB1 expression.

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عنوان ژورنال:

دوره 16  شماره 

صفحات  -

تاریخ انتشار 2017