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LncRNAs are increasingly verified to be aberrantly expressed in cancers. The abnormal expression of lncRNAs has turned out to be closely related to tumorigenesis or tumor progression. It has been reported that lncRNA OPI5-AS1 serves as a crucial regulator in tumors. However, the specific function of OIP5-AS1 on the progression of lung adenocarcinoma is still uncertain. In this paper, we mainly elucidated that OIP5-AS1 exerts oncogenic functions in human lung adenocarcinoma through targeting miR-448. We inspected that the expression of OIP5-AS1 was definitely high in lung adenocarcinoma tissues and cells, while miR-448 was sluggishly expressed in lung adenocarcinoma. OIP5-AS1 and miR-448 was negatively related to each other, the result was obtained from Pearson correlation analysis. We discovered a fact that OIP5-AS1 could directly sponge miR-448 through using dual luciferase reporter assay, RIP assay and RNA pull-down assay. Cell proliferation, migration and invasion were restrained after we disrupted the expression of OIP5-AS1 in lung adenocarcinoma. We also certified that OIP5-AS1 could sponge and regulate miR-448 to affect cell function in lung adenocarcinoma. MiR-448 could target Bcl-2 and affect the expression of Bcl-2. Then, we discovered that the expression of OIP5-AS1 and Bcl-2 was positively related. So we affirmed that lncRNA OIP5-AS1 modulated the expression of Bcl-2 by targeting miR-448 in lung adenocarcinoma cells.

The synergistic effect of pH and heating on the structure, aggregation behaviour and gel properties of myofibrillar protein (MP) in mirror carp (Cyprinus carpio) was evaluated. The surface hydrophobicity of the control at pH 5.0 (143.6 ± 0.3 μg) was significantly higher than that of other samples (P 0.05). Under the same pH conditions, the decrease in total sulfhydryl content of all samples during the heating process demonstrated that covalent/non-covalent cross-linking occurred between proteins due to heat input. Moreover, the decrease in solubility and the increase in turbidity of all samples verified the fact of MP aggregation, and the changes in the elasticity index (EI) and macroscopic viscosity index (MVI) also indicated a decrease in MP fluidity upon heating treatment. Therefore, the aggregation of MP was affected by pH and heating, and the optimal three-dimensional network structure and gel properties could be formed at pH 6.0 and above 70 °C.

Sex steroid hormones have been reported to induce inflammation causing dysregulation of cytokines in prostate cancer cells. However, the underlying epigenetic mechanism has not well been studied. The objective of this study was to evaluate the effect of sex steroid hormones on epigenetic DNA methylation changes in prostate cancer cells using a signature PCR methylation array panel that correspond to 96 genes with biological function in the human inflammatory and autoimmune signals in prostate cancer. Of the 96-gene panel, 32 genes showed at least 10% differentially methylation level in response to hormonal treatment when compared to untreated cells. Genes that were hypomethylated included CXCL12, CXCL5, CCL25, IL1F8, IL13RAI, STAT5A, CXCR4 and TLR5; and genes that were hypermethylated included ELA2, TOLLIP, LAG3, CD276 and MALT1. Quantitative RT-PCR analysis of select genes represented in a cytokine expression array panel showed inverse association between DNA methylation and gene expression for TOLLIP, CXCL5, CCL18 and IL5 genes and treatment of prostate cancer cells with 5'-aza-2'-deoxycytidine with or without trichostatin A induced up-regulation of TOLLIP expression. Further analysis of relative gene expression of matched prostate cancer tissues when compared to benign tissues from individual patients with prostate cancer showed increased and significant expression for CCL18 (2.6-fold; p0.001), a modest yet significant increase in IL5 expression (1.17-fold; p=0.015), and a modest increase in CXCL5 expression (1.4-fold; p=0.25). In conclusion, our studies demonstrate that sex steroid hormones can induce aberrant gene expression via differential methylation changes in prostate carcinogenesis.

Long non-coding RNA (lncRNA) is actively transcribed from human genome and has been considered to participate in many processes of various cancers. The purpose of this study was to investigate the expression of LncRNA AFAP1-AS1 and its prognostic value in NSCLC. LncRNA AFAP1-AS1 expression was detected by qRT-PCR which demonstrated that the expression was significantly increased in tumor tissues compared with the adjacent non-cancerous tissues and healthy tissues. The clinical stage, smoking history, infiltration degree, lymph node metastasis and distant metastasis were all proved to impact the expression of LncRNA AFAP1-AS1 (P