LINC00664/miR-411-5p/KLF9 feedback loop contributes to the human oral squamous cell carcinoma progression.

OBJECTIVES

Oral squamous cell carcinoma (OSCC) is one of the most aggressive head and neck cancers with high incidence. Multiple studies have revealed that long non-coding RNAs (lncRNAs) play pivotal roles in tumorigenesis. However, the role of long intergenic non-protein coding RNA 664 (LINC00664) on the progression of OSCC was still unclear.

SUBJECTS AND METHODS

In this study, the expression of LINC00664 in OSCC tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The functional role of LINC0664 was estimated by cell counting kit-8 (CCK-8), transwell assays, Western blot in vitro, and xenograft tumor model in vivo. The regulatory mechanism was investigated by RNA-binding protein immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), and luciferase reporter assays.

RESULTS

LINC00664 was found to be upregulated in OSCC tissues and cell lines and was associated with poor prognosis of OSCC patients. LINC00664 knockdown suppressed OSCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Moreover, Kruppel like factor 9 (KLF9) enhanced LINC00664 expression at transcription level. Interestingly, LINC00664 upregulated KLF9 expression by sponging miR-411-5p. In addition, knockdown of LINC00664 restrained tumor growth of OSCC in vivo.

CONCLUSION

Our study identified the oncogenic roles of LINC00664 in OSCC tumorigenesis and EMT via KLF9/LINC00664/miR-411-5p/KLF9 feedback loop, which provides new perspectives of the potential therapeutic target for OSCC.