Opa interacting protein 5 promotes metastasis of nasopharyngeal carcinoma cells by promoting EMT via modulation of JAK2/STAT3 signal.

OBJECTIVE

Opa interacting protein 5 (OIP5), as a tumor promoter gene, has emerged as a regulator in several types of tumors. However, the role of OIP5 in nasopharyngeal carcinoma (NPC) has not been reported. In this study, we aimed to explore the expression and biological function of OIP5 in NPC.

PATIENTS AND METHODS

The lung cancer datasets GSE12452 and GSE53819 were downloaded from the Gene Expression Omnibus (GEO) repository. Real-time-Polymerase Chain Reaction (RT-PCR) was performed to detect the expression levels of OIP5 mRNA. Cell Counting Kit-8 (CCK-8), colony-formation assay, wound healing assay and transwell assay were conducted to measure cells' proliferation, migration and invasion. Flow cytometry was used for analysis of apoptosis. Western blot assays were used to assess the effects of OIP5 on EMT and JAK2/STAT3 pathway.

RESULTS

The up-regulation of OIP5 mRNA was observed in NPC tissues from both GSE12452 and GSE53819. The results of RT-PCR also showed that the expression of OIP5 mRNA was significantly up-regulated in several NPC cell lines compared to normal nasopharyngeal cells. Furthermore, lost-function assay revealed that the knockdown of OIP5 markedly suppressed NPC cells proliferation, migration and invasion, and promoted cell apoptosis. In addition, the results of Western blot showed that silencing of OIP5 suppressed the EMT in NPC cell line. Meanwhile, the knockdown of OIP5 remarkably decreased the expression of p-JAK2 and p-STAT3 protein in both CNE1 and SUNE1 cells.

CONCLUSIONS

Our data indicated that OIP5 was highly expressed in NPC and promoted NPC progression by modulating JAK2/STAT3; our results shed light on utilizing OIP5 as a potential novel therapeutic target for the treatment of NPC.