MicroRNA-210 targets FBXO31 to inhibit tumor progression and regulates the Wnt/ß-catenin signaling pathway and EMT in esophageal squamous cell carcinoma.

Evidence from previous studies showed that the dysregulation of microRNA (miR) is frequently associated with tumor progression. The aberrant miR-210 expression has been identified in a variety of tumors. However, its biological roles in esophageal squamous cell carcinoma (ESCC) still need further elucidation. Thus, in the current study we explore the roles of miR-210 in ESCC progression. The findings of our study reveal that miR-210 is down-regulated in ESCC, which indicates poor prognosis and aggressive tumor progression. Moreover, miR-210 restoration was found to enhance ESCC viability, invasion, and migration abilities. F-Box only protein 31 (FBXO31) was confirmed to be one of the targets of miR-210 in ESCC cells. Results also revealed that miR-210 played crucial roles in regulating ESCC cell epithelial-mesenchymal transition (EMT) and Wnt/ß-catenin signaling. In conclusion, data show that miR-210 serves as an anti-ESCC miR via down-regulation of FBXO31 and regulation of EMT and Wnt signaling, suggesting that the miR-210/FBXO31 axis may function as promising therapeutic targets and effective prognostic markers for ESCC patients.

miR-205 regulation of ICT1 has an oncogenic potential via promoting the migration and invasion of gastric cancer cells.

Immature colon carcinoma transcript-1 (ICT1) is a newly identified oncogene, which regulates mobility, apoptosis, cell cycle progression and proliferation of cancer cells. Nevertheless, the role of ICT1 and its clinical significance in gastric cancer (GC) is largely uncovered. Here, we found that ICT1 displayed higher expression in GC tissues compared to corresponding tumor-adjacent tissues. Further investigation confirmed ICT1 overexpression in GC cell lines. Clinical data disclosed that high ICT1 expression correlated with distant metastasis and advanced tumor-node-metastasis (TNM) stage. The Cancer Genome Atlas (TCGA) data further demonstrated that GC tissues with metastasis showed a significant higher level of ICT1 compared to those without metastasis. Furthermore, ICT1 overexpression notably predicted poor prognosis of GC patients. Functionally, we demonstrated that ICT1 knockdown suppressed invasion and migration of MGC-803 and BGC-823 cells in vitro. ICT1 overexpression promoted the mobility of SGC-7901 cells. Mechanistically, microRNA-205 (miR-205) was recognized as a direct down-regulator and inversely modulated ICT1 abundance in GC cells. miR-205 expression was down-regulated and negatively associated with ICT1 level in GC tissues. Underexpression of miR-205 indicated an obvious shorter survival of GC patients. miR-205 overexpression inhibited migration and invasion of MGC-803 cells, while these inhibitory effects were reversed by ICT1 restoration. Taken together, we have the earliest evidence that miR-205 regulation of ICT1 functions as an oncogene and prognostic biomarker in GC.