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The long noncoding RNASBF2-AS1 can promote the occurrence and development of many kinds of tumours, but its role in oesophageal squamous cell carcinoma (ESCC) is unknown. We found that SBF2-AS1 was up-regulated in ESCC, and its expression was positively correlated with tumor size (P = 0.0001), but was not related to gender, age, TNM stage, histological grade, and lymphnode metastasis (P > 0.05). It was further found that the higher the expression of SBF2-AS1, the lower the survival rate. COX multivariate analysis showed that the expression of SBF2-AS1 was an independent prognostic factor. Functional experiments show that inhibition of SBF2-AS1 can inhibit the proliferation of ESCC through in vivo and in vitro, and overexpression of SBF2-AS1 can promote the proliferation of ESCC and inhibit its apoptosis. In mechanism, SBF2-AS1/miR-338-3P, miR-362-3P/E2F1 axis are involved in the regulation of ESCC growth. In general, SBF2-AS1 may be used as ceRNA to combine with miR-338-3P and miR-362-3P to up-regulate the expression ofE2F1, and ultimately play a role in promoting cancer. It may be used as a therapeutic target and a biomarker for prognosis. [ABSTRACT FROM AUTHOR]

Background/Aims: The HOX transcript antisense intergenic RNA (HOTAIR), a long noncoding RNA (lncRNA), plays an important role in the pathogenesis and progression of multiple tumors. The aim of the present study was to evaluate whether common single nucleotide polymorphisms (SNPs) in HOTAIR are related to hepatocellular carcinoma (HCC) susceptibility in a Chinese population. Methods: We genotyped three SNPs of HOTAIR in a hepatocellular carcinoma (HCC) case-control study, including 482 cases and 520 control subjects. SNPs were genotyped using real-time polymerase chain reaction (RT-PCR). Associations between gene polymorphisms and HCC were evaluated using multiple logistic regression analysis. The allelespecific effects on HOTAIR expression in HCC were confirmed by real time quantitative PCR and luciferase activity assays. The influence of HOTAIR SNPs on the proliferation of HCC cells was evaluated using a CCK-8 assay. Results: Significant associations were observed between the HOTAIR rs920778 C>T polymorphism and HCC risk (TT versus CC: OR = 1.634, 95% CI =1.028- 2.598, P = 0.046) and the allelic model (allele T versus allele C: OR =1.293, 95% CI = 1.060- 1.577, P = 0.011). However, no statistically significant differences of rs4759314 and rs1899663 genotypes were observed between patients and controls (both P > 0.05). The increased risk for rs920778 TT genotype carriers was more evident in a sub-group of drinkers (OR = 3.103, 95% CI = 1.151-8.368, p=0.025) and in people positive for HBV infection (OR = 2.885, 95% CI = 1.086-7.663, p=0.034). RT-PCR and luciferase activity assay confirmed that the rs920778 TT genotype induced significantly higher HOTAIR levels than did the CC genotype (P < 0.05). CCK-8 assays and colony formation assays demonstrated that the rs920778 TT genotype had a higher proliferation rate of HCC cells than did the CC genotype (P < 0.05). Conclusion: These results suggest that SNP rs920778 of HOTAIR acts as a potential biomarker for predicting hepatocellular carcinoma, and further studies are warranted to confirm these findings. [ABSTRACT FROM AUTHOR]

BRAF activated non-coding RNA (BANCR), a long non-coding RNA (lncRNA), is crucial for cell migration in melanoma cells and non-small cell lung cancer (NSCLC) cells. However, little is known regarding the role of this gene in the proliferation of colorectal cancer. Therefore, we investigated the involvement of BANCR in the proliferation of colorectal cancer cells. In this study, we show that BANCR expression was significantly down-regulated in colorectal cancer tissues compared with normal tissues, and overexpression of BANCR suppressed colorectal cancer cell growth in vitro and in vivo. We also determined that pCDNA-BANCR-mediated colorectal cancer cell proliferation was associated with induction of G0/G1 cell-cycle arrest and apoptosis enhancement through regulation of p21, and its effects were most likely posttranscriptional. Taken together, our findings suggest that down-regulation of BANCR contributes to the proliferation of colorectal cancer cells, at least in part, through the regulation of p21 protein. [ABSTRACT FROM AUTHOR]