Background. Actin filament-associated protein 1-antisense RNA 1 (AFAP1-AS1) plays an important role in the development and progression of several human cancers. However, its biological function in gastric cancer (GC) progression is still unknown. Methods. We used qRT-PCR to detect the relative expression of AFAP1-AS1 in GC tissues and cell lines. The loss-of-function assays were conducted to detect the effect of AFAP1-AS1 on GC development. Bioinformatics analysis, luciferase reporter gene analysis, and RIP analysis were used to identify and validate target genes of AFAP1-AS1. Finally, rescue tests were performed to confirm the influence of the AFAP1-AS1-miR-155-5p-FGF7 axis on GC development. Results. AFAP1-AS1 was upregulated in GC tissues and cell lines and was closely correlated with poor prognosis of GC patients. AFAP1-AS1 knockdown inhibited proliferation, migration, and invasion of GC cells, indicating that AFAP1-AS1 acts as an oncogene in GC. Bioinformatics analysis, dual-luciferase reporter gene detection, and RIP assays validated that AFAP1-AS1 directly interacts to miR-155-5p and could positively affect cell proliferation, migration, and invasion by regulation of the expression of miR-155-5p and FGF7. Further rescue assays revealed that AFAP1-AS1 promotes cell proliferation and metastasis through the miR-155-5p/FGF7 axis in GC. Conclusions. AFAP1-AS1 might be an oncogenic lncRNA that promoted GC progression by acting as a competing endogenous RNA (ceRNA) that regulates the expression of FGF7 through sponging miR-155-5p, suggesting that AFAP1-AS1 may be a novel potential therapeutic target for GC.

DNA hypermethylation of secreted frizzled-related protein 2 (SFRP2) gene associated with the Wnt signaling pathway has been studied previously. However, the risk size and changing rules between colorectal cancer (CRC) and SFRP2 hypermethylation from precancerous disease to CRC remain unclear. The aim of work was therefore to investigate the risk size and changing rule based on detections on large numbers of tissue and feces samples. Association study and meta-analysis were performed to analyze the risk size of SFRP2 hypermethylation in tissue and fecal detections from 2,912 samples, including 1,436 patients with CRC, 866 patients with colon adenomas or polyps, and 610 samples with both normal controls. Based on normal controls as standard reference, the analysis showed that SFRP2 hypermethylation in CRC and adenoma tissues had a significantly higher risk with 92.81 (28.76-299.45) and 22.46 (4.13-122.04) odds ratio (OR) (95 % confidence interval (CI)) respectively, and that the risk sizes of SFRP2 hypermethylation in CRC and adenoma patients were 41.86 (18.91-92.67) and 11.76 (6.98-19.84) of OR (95 % CI) in fecal samples, and that the OR risk in both tissue and fecal samples increased significantly to 70.35 and 30.10 from precancerous disease (adenoma or polyp) to CRC. There were significant differences between tissue and fecal hypermethylation frequency. On the basis of the hypermethylation frequency of colorectal tissue, the coincidence rates of fecal hypermethylation in CRC and colorectal adenoma were 0.89 and 0.9, respectively. The risk size of SFRP2 hypermethylation from normal control to adenoma or polyp as well as from adenoma or polyp to CRC increased gradually in both tissue and feces. Therefore, SFRP2 hypermethylation is an important biomarker both in noninvasive diagnosis in feces detection and in colon tissue.

INTRODUCTION: In patients with compensated advanced chronic liver disease (cACLD), the invasive measurement of hepatic venous pressure gradient is the best predictor of hepatic decompensation. This study aimed at developing an alternative risk prediction model to provide a decompensation risk assessment in cACLD. METHODS:Patients with cACLD were retrospectively included from 9 international centers within the Portal Hypertension Alliance in China (CHESS) network. Baseline variables from a Japanese cohort of 197 patients with cACLD were examined and fitted a Cox hazard regression model to develop a specific score for predicting hepatic decompensation. The novel score was validated in an external cohort (n 5 770) from 5 centers in China, Singapore, Korea, and Egypt, and was further assessed for the ability of predicting clinically significant portal hypertension in a hepatic venous pressure gradient cohort (n 5 285).

The susceptibility of secreted frizzled-related protein 2 (SFRP2) methylation in colorectal cancer (CRC) has been studied previously. The aim of this study was to determine the risk sizes and variation trends of SFRP2 methylation in CRC development in Chinese populations. Subgroup meta-analysis and the least-squares curve-fitting method were carried out to analyze the risk of SFRP2 methylation in tissue, feces, and blood detection from 2221 samples, including a total of 1103 cases of CRC, 459 cases of adenoma, 257 cases of polyps, and 402 controls. The data showed that odds ratios (95% confidence intervals) between CRC and controls for tissue, feces, and blood detection were 334.01 (104.42-1068.39), 63.76 (20.62-197.63), and 133.75 (18.32-976.32), respectively. There were also significant differences between tissue and feces or blood as well as between feces and blood methylation frequency. These results showed that the risk size in tissue was much greater than that in feces and that in blood. The results pointed out that three curves in tissue, feces, and blood detection described the variation trends of methylation incidence from the control to polyp, to adenoma and to CRC, and that the variation trend of the risk size of SFRP2 methylation was synchronized with the histological evolution process of CRC. The variation trend of the risk size of SFRP2 methylation incidence is consistent with the histological evolution process of CRC. The susceptibility to SFRP2 methylation is an important biomarker in the study of early diagnosis of CRC and high-risk patients.

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