Background
Long non-coding RNAs (lncRNAs) have been widely confirmed to modulate many tumorigeneses, including NPC. However, the exact roles of cancer susceptibility candidate 9 (CASC9) in nasopharyngeal carcinoma (NPC) and its underlying mechanisms have not been fully established.
Conclusion
CASC9 knockdown inhibited cell migration and invasion but increased cell apoptosis in NPC cells by regulating miR-145, providing a novel insight for the treatment of NPC.
Methods
qRT-PCR was used to determine CASC9 and miR-145 expressions. Cell apoptosis, migration, and invasion were determined by flow cytometry and transwell assays, respectively. The protein expressions of BAX, Bcl-2, MMP 9, and MMP 2 were measured by western blot. The possible binding sites between miR-145 and CASC9 were predicted by the starBase v2.0 online database and verified by a luciferase report and an RNA immunoprecipitation (RIP) assay. A xenograft tumor model was established to confirm the effects of CASC9 in NPC progression in vivo.
Results
The expression level of CASC9 was upregulated in NPC tissues and cells. The knockdown of CASC9 evidently suppressed migration and invasion but promoted apoptosis in NPC cells. In addition, the inhibition of CASC9 evidently increased the BAX protein level and inhibited the expression of the Bcl-2, MMP 9, and MPP2 proteins in NPC cells. Moreover, miR-145 was directly bound to CASC9, and its inhibition reversed the inhibitory effect of CASC9 knockdown on the progression of NPC. Furthermore, the expression of miR-145 was decreased and negatively associated with CASC9 in NPC tissues and cells. Also, the knockdown of CASC9 inhibited tumor growth in vivo.