MicroRNA181c inhibits prostate cancer cell growth and invasion by targeting multiple ERK signaling pathway components.

摘要: Background The ERK signaling pathway is frequently deregulated in tumorigenesis, mostly by classical mechanisms such as gene mutation of its components (eg, RAS and RAF). However, whether how multiple key are regulated microRNAs not clear. Methods We firstly predicted post-transcriptional regulation the miR181c through bioinformatics analysis, then confirmed dual luciferase reporter assays Western blot analysis. biological effects on prostate cancer cell proliferation, apoptosis, migration, invasion were measured CCK-8 assay, flow cytometry, wound scratch transwell assays. Results post-transcriptionally members pathway, including extracellular signal-regulated kinase 2 (ERK2), ribosomal S6 (RSK2), serum response factor (SRF), FBJ murine osteosarcoma viral oncogene homolog (c-Fos). Ectopic expression mimics effectively suppressed invasion, but promoted apoptosis. Furthermore, treatment combined with multi-kinase inhibitor sorafenib significantly enhanced these anti-tumor effects. Conclusions Downregulation results promotes growth metastasis.