Integrative profiling analysis identifies the oncogenic long noncoding RNA DUXAP8 in oral cancer.

A growing number of studies have revealed the critical roles of long noncoding RNAs (lncRNAs) in the tumorigenesis and cancer progression. Recently, next-generation sequencing technologies combined with bioinformatic have demonstrated that a great number of dysregulated lncRNAs are associated with diverse cancers. However, lots of lncRNAs' function and their underlying molecular mechanisms in oral carcinoma (OC) cancer remain unclear. In this study, we performed integrative lncRNA profiling analysis using the TCGA RNA sequencing data and gene microarray data from Gene Expression Omnibus to identify more OC associated lncRNAs. A total of 619 differentially expressed lncRNAs were identified between the five data sets, and only the double homeobox A pseudogene 8 (DUXAP8) was screened among the up-regulated lncRNAs in all the five groups. Meanwhile, univariate Cox regression analyses disclosed that some lncRNAs are associated with the outcome of OC patients, such as DUXAP8, LINC00152, MIR4435-2HG and LINC00582. Furthermore, we uncovered that silenced DUXAP8 expression exerted suppressive impact on the proliferation of OC cells through interacting with histone-lysine N-methyltransferase enzyme Enhancer of zeste homolog 2 (EZH2) and repressing KLF2 expression. In a word, we identified a lot of unreported OC associated lncRNAs, which may provide a useful resource of lncRNAs for other studies.

Inhibition of miR­21 promotes cell apoptosis in oral squamous cell carcinoma by upregulating PTEN.

MicroRNA­21 (miR­21) has been identified as an oncogene and confirmed to serve an important role in carcinogenesis in various types of cancer. However, the effect and mechanism of miR­21 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. In the present study, miR­21 inhibitor and empty vector were transfected into OSCC cells, and non­transfected cells were used as a blank control. The results indicated that when compared with the control and scramble groups, miR­21 inhibitor suppressed the expression of miR­21. Conversely, phosphatase and tensin homolog deletion on chromosome 10 (PTEN) was markedly upregulated, and a dual luciferase reporter assay revealed PTEN to be a target gene of miR­21. Furthermore, miR­21 inhibitor decreased the proliferation and invasion and enhanced the apoptosis of OSCC cells. There was no significant difference in cell proliferation, invasion and apoptosis between the control and scramble groups. The present data suggested that there may be a regulatory loop between miR­21 and PTEN, and that miR­21 inhibition affected the proliferative, invasive and apoptotic abilities of OSCC cells. These findings indicate that miR­21 may be a possible novel target in the treatment of OSCC.