LncRNA Opa interacting protein 5‐antisense RNA 1 (OIP5‐AS1) promotes the migration, invasion and epithelial‐mesenchymal transition (EMT) through targeting miR‐147a/insulin‐like growth factor 1 receptor (IGF1R) pathway in cervical cancer tissues and cell model
Abstract
Background
Two factors involved in regulation, long noncoding RNA Opa interacting protein 5‐antisense RNA 1 (lncRNA OIP5‐AS1) and microRNA‐147a, were found in cervical cancer. Therefore, the investigation of the specific regulation of miR‐147a by OIP5‐AS1 was performed in cervical cancer.
Method
The cervical cancer tissues were collected from patients with cervical cancer (n = 50). The expression of OIP5‐AS1, miR‐147a, proteins in epithelial‐mesenchymal transition (EMT) process and insulin‐like growth factor 1 receptor (IGF1R) were measured by quantitative real‐time polymerase chain reaction (qRT‐PCT) or western blotting. Cell motility and the relationship between OIP5‐AS1 and miR‐147a were detected or analyzed by wound healing test, Transwell assay, dual‐luciferase reporter assay, RNA binding protein immunoprecipitation assay or Pearson correlation in OIP5‐AS1, or miR‐147a over‐expressed and/or suppressed cervical cancer cells.
Results
OIP5‐AS1 showed the high‐expression and miR‐147a showed the low‐expression in tumor tissues collected from patients with cervical cancer and cell lines Hela, CaSki, Siha, and ME‐180. The low‐expression of OIP5‐AS1 suppressed the motility of Caski cells, as well as up‐regulated the level of E‐cadherin, which a key protein in EMT. There were targeting sites between miR‐147a and OIP5‐AS1. OIP5‐AS1 induced the down‐regulation of miR‐147a, so miR‐147a was inversely correlated with OIP5‐AS1. The down‐regulation of miR‐147a increased IGF1R and E‐cadherin, and these increases were alleviated by OIP5‐AS1 knockdown.
Conclusion
LncRNA OIP5‐AS1 promotes the migration, invasion and EMT of cervical cancer cells via targeting miR‐147a/IGF1R pathway.