Oral squamous cell carcinoma (OSCC) is one of the most aggressive and lethal malignancies affecting the head and neck region with a general 5-year survival rate about 50%. Long non-coding RNAs (lncRNAs) are believed to participate in diverse biological processes and are emerging as convenient and minimally invasive diagnostic/prognostic/therapeutic markers. The aim of this study was to explore CEBPA-AS1 role and mechanism in OSCC tumorigenesis. In this study, CEBPA-AS1 localized in the cytoplasm and the peri-nuclear cellular compartment functioning as a potential oncogene up-regulated in OSCC was correlated with poor differentiation, lymph node metastasis and high clinical stage, which made it considered to be a prognostic biomarker. Silence of CEBPA-AS1 inhibited OSCC cells proliferation and induced cells apoptosis, migration and invasion by targeting CEBPA and via a novel pathway CEBPA/Bcl2. Our findings provided the first evidence for the lncRNA CEBPA-AS1 regulatory network in OSCC tumorigenesis, which might be helpful to improve the effects of clinical treatment in OSCC.

Oral squamous cell carcinoma is a common and lethal malignancy affecting the head and neck region. CCAT2 (colon cancer-associated transcript 2) gene is affiliated with long non-coding RNAs, which are often found to have important regulatory roles in cancers. This study aims to assess the expression and clinical significance of CCAT2 gene, identify its malignant biological behaviors, and explore the possible mechanisms in oral squamous cell carcinoma. CCAT2 expression was detected by quantitative real-time polymerase chain reaction, and its relationship with clinical factors was assayed using the Kaplan-Meier survival curve. The biological behaviors of CCAT2 and its potential mechanisms in oral squamous cell carcinoma were explored by the combined use of CCAT2 knockdown technology and the Wnt/β-catenin pathway agonist lithium chloride (LiCl). Our results showed that CCAT2 functioning as a potential oncogene was upregulated in oral squamous cell carcinoma. CCAT2 with high expression level was correlated with poor differentiation, higher T stage, and clinical stage, which made CCAT2 to be a prognostic biomarker in oral squamous cell carcinoma. LiCl-activated Wnt/β-catenin signaling pathway could partly restore the CCAT2-mediated malignant biological behaviors of oral squamous cell carcinoma cells by suppressing β-catenin, CCND1, and MYC and activating glycogen synthase kinase 3 beta expression. These findings might assist in the discovery of novel potential diagnostic and therapeutic target for oral squamous cell carcinoma, thereby improve the effects of clinical treatment in patients.

Objective : Human brain glioma is the most malignant primary intracranial tumor, which has poor prognosis and high mortality. Long noncoding RNAs are considered to take part in cellular phenotypes and are emerging as diagnostic and prognostic biomarkers of glioma. This study will research the effects of Small Nucleolar RNA Host Gene 5 (SNHG5) gene on malignant cellular phenotypes in glioma and explore the possible mechanisms. Materials and Methods : The expression level of SNHG5 was examined using quantitative Real-time PCR in glioma tissues and cell lines. Loss-of-function experiments of SNHG5 together with Enhanced Cell Counting Kit-8, flow cytometry and cell invasion assay were used to investigate the effects of SNHG5 on malignant cellular phenotypes of glioma cells. Finally, luciferase assay and western blotting were applied to determine the activity of WNT/CTNNB1 signaling pathway. Results : SNHG5 gene was high-expressed in glioma tissues and cell lines. Knockdown of SNHG5 gene depressed cell proliferation and invasiveness as well as promoted the apoptosis of U251 and U87 cells. In addition, online database analysis showed SNHG5 was closely related to Wnt/CTNNB1 signaling pathway. Knockdown of SNHG5 inactivated Wnt/CTNNB1 signaling pathway, and the activating of Wnt/CTNNB1 signaling pathway partly restored the influences of SNHG5 knockdown on malignant cellular phenotypes of U251 and U87 cells. Conclusion : SNHG5 gene was high-expressed in glioma, knockdown of SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway.

These findings suggest a negative correlation between TUSC7 expression and TMZ resistance and provide a mechanism and rationale for targeting TUSC7 in the treatment of GBM.

In genitourinary system, bladder cancer (BC) is the most common and lethal malignant tumor, which most common type is bladder urothelial carcinoma (BUC). Long non-coding RNA (lncRNA) Taurine Up-Regulated 1 (TUG1) gene is high-expressed in several malignant tumors, including BC. In this study, over-expression of TUG1 was found in BUC tissues and cell line resistant to doxorubicin (Dox). Knockdown of TUG1 inhibited the Dox resistance and promoted the cytotoxicity induced by Dox in T24/Dox cells. TUG1 knockdown also depressed the Wnt/β-catenin pathway, and the activation the Wnt/β-catenin pathway partly reversed the inhibitory effects of TUG1 knockdown on Dox resistance in T24/Dox cells. In conclusion, up-regulation of lncRNA TUG1 was related with the poor response of BUC patients to Dox chemotherapy, knockdown of TUG1 inhibited the Dox resistance of BUC cells via Wnt/β-catenin pathway. These findings might assist in the discovery of novel potential diagnostic and therapeutic target for BUC, thereby improve the effects of clinical treatment in patients.