Long noncoding RNA (lncRNA) differentiation antagonizing nonprotein coding RNA (DANCR) plays important regulatory roles in many solid tumors. However, the effect of DANCR in glioma progression and underlying molecular mechanisms were not entirely explored. In the present study, we determined the expression of DANCR in glioma tissues and cell lines using qRT-PCR and further defined the biological functions. Furthermore, we used luciferase reporter assay, Western blot, and RNA immunoprecipitation (RIP) to explore the underlying mechanism. Our results showed that DANCR was significantly up-regulated in glioma tissues and cell lines (U251, U118, LN229, and U87MG). High DANCR expression was correlated with advanced tumor grade. Inhibition of DANCR suppressed the glioma cells proliferation and induced cells arrested in the G0/G1 phase. In addition, we verified that DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression. The present study demonstrated that DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma, and DANCR might potentially serve as a therapeutic target for the treatment of glioma patients.

Renal cell carcinoma (RCC) is among the most common subtype of kidney cancers, and the current therapeutic strategies are not efficient. Natural killer (NK) cells are biological agents that can induce apoptosis in a wide range of cancer cells. However, most of RCC patients exhibit resistance against the action of NK cells due to unknown mechanisms. This study is aimed to identify a biomarker that can predict the response of RCC cells to NK cell treatment. We collected 82 RCC patients and 19 healthy volunteers to detect the expression of miR-183 in blood by qPCR assays. The results revealed that serum miR-183 is significantly higher in RCC patients than in healthy controls, and its level is positively associated with the grading of RCC. Furthermore, (51)Cr release assays indicated that the primary RCC cells with low serum miR-183 expression are more sensitive to the cytotoxicity of NK cells. Collectively, we demonstrated that serum miR-183 can be used to predict the response of RCC cells to the cytotoxicity induced by NK cells.

We conducted this case-control study to assess the role of vascular endothelial growth factor (VEGF) -2578C/A, +460T/C, +1612G/A, +936C/T, and -634G/C polymorphisms in the development of renal cell carcinoma (RCC), and analyzed the association of gene polymorphisms with demographic and clinical characteristics of RCC. This study included 412 consecutive primary RCC patients and 824 controls. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to detect VEGF -2578C/A, +460T/C, +1612G/A, +936C/T, and -634G/C polymorphisms. Compared with the control subjects, the RCC cancer cases were more likely to have a habit of cigarette smoking, and suffered from hypertension and diabetes. Conditional logistic regression analysis showed that individuals carrying the AA genotype of -2578C/A were more likely to greatly increase risk of RCC, and the CC genotype of +460T/C revealed a significant association with increased risk of RCC. The CA + AA genotype of -2578C/A had a significantly increased risk of RCC in ever cigarette smokers, and individuals who suffered from hypertension and diabetes. TC + CC genotype of +460T/C was significantly associated with the elevated risk of RCC in those suffered from hypertension and diabetes. Our study suggests that -2578C/A and +460T/C polymorphisms of VEGF modulate the risk of developing RCC in Chinese population.

MicroRNAs (miRNAs) have been shown to have a significant role in the progression of several types of cancer, including oral squamous cell carcinoma (OSCC). However, the biological function and regulatory mechanisms of miRNAs in OSCC remain to be fully elucidated. The aim of the present study was to investigate the role of miRNAs in OSCC and the relevant mechanism. Using a microarray, it was found that miRNA (miR)-199a-5p was one of the most downregulated miRNAs in OSCC tissues. A low expression of miR-199a-5p was closely associated with tumor differentiation, lymph node metastasis, tumor-node-metastasis stage, and overall survival rate. Functionally, the overexpression of miR-199a-5p suppressed cell proliferation, induced G0/G1 cell cycle arrest, and promoted the apoptosis of Tca8113 and SCC-4 cells. Subsequently, inhibitor of nuclear factor-κB (NF-κB) kinase β (IKKβ), an important regulator of NF-κB activation, was identified as a direct target of miR-199-5p. An inverse correlation was found between miR-199a-5p and IKKβ in tumor tissues. Further investigations revealed that the overexpression of IKKβ efficiently abrogated the influences caused by the overexpression of miR-199a-5p. It was also found that the miR-199a-5p-mediated anticancer effects were dependent on the inhibition of NF-κB activation. These findings indicate that miR-199a-5p functions as a tumor suppressor through regulation of the NF-κB pathway by targeting IKKβ in OSCC.

MicroRNAs (miRs) are small, non-coding RNAs that can act as oncogenes or tumor suppressor genes in human cancer. Recent studies have revealed that miR-199a-5p is abnormally expressed in various types of human cancer; however, the potential role of miR-199a-5p in oral squamous cell carcinoma (OSCC) remains elusive. The present study investigated the role of miR-199a-5p in OSCC cells and explored the potential molecular mechanism. Reverse transcription-quantitative polymerase chain reaction was used to measure miR-199a-5p expression in OSCC tissues and adjacent normal oral epithelial tissues. Cell invasion and migration were evaluated using Transwell invasion and wound-healing assays in OSCC cells post-transfection with miR-199a-5p mimics or negative control mimics. In addition, a luciferase reporter assay was conducted to identify the target gene of miR-199a-5p in OSCC cells. The results demonstrated that miR-199a-5p expression was significantly downregulated in OSCC tissues and cell lines, and was associated with tumor progression in OSCC. Furthermore, overexpression of miR-199a-5p inhibited cell invasion and migration, and blocked the epithelial-mesenchymal transition (EMT) cascade. Notably, the results revealed that the EMT-related transcription factor SRY-box 4 (SOX4) was a direct target gene of miR-199a-5p, as determined by the direct binding of miR-199a-5p with the 3′-untranslated region of SOX4. In addition, knockdown of SOX4 by small interfering RNA-SOX4 suppressed proliferation, migration and invasion of OSCC cells. Conversely, overexpression of SOX4 rescued the suppressive effects of miR-199a-5p on cell migration and invasion. Collectively, these data indicated that miR-199a-5p may inhibit the migration and invasion of OSCC cells via targeting the EMT-related transcription factor SOX4, thus suggesting that miR-199a-5p may serve as a prognostic biomarker and therapeutic target in the treatment of OSCC.