Erratum: Silibinin inhibits the migration and invasion of human gastric cancer SGC7901 cells by downregulating MMP-2 and MMP-9 expression via the p38MAPK signaling pathway.

[This corrects the article DOI: 10.3892/ol.2017.7080.].

The clinicopathological characteristics of gastric polyps and the relationship between fundic gland polyps, Helicobacter pylori infection, and proton pump inhibitors.

BACKGROUND: To explore the clinical characteristics of different types of gastric polyps and the relationship between fundic gland polyps, Helicobacter pylori (HP) infection, and proton pump inhibitor (PPI) use. METHODS: The clinical data of 186 patients diagnosed with gastric polyps under endoscopy were selected for retrospective analysis, and the clinical data, gastroscopy, polyp histopathology, HP infection, and PPI usage of all subjects were analyzed. RESULTS: Among the 186 patients with gastric polyps, there were significantly more women (131 cases) than men (55 cases), with a ratio of 2.38:1. PPIs were used in 78% of cases for more than 5 years. The pathological types of patients with gastric polyps in this study were fundic gland polyps, hyperplastic polyps, inflammatory fibrous polyps, and adenomatous polyps. Fundic gland polyps were mainly located in the fundus and gastric body, while hyperplastic polyps were mostly located in the gastric body (P<0.05). The positive rate of HP infection in patients with fundic gland polyps was significantly lower than that in patients with other types of polyps (P<0.05). In patients with long-term use of PPIs, the incidence of fundic gland polyps increased significantly (P<0.05). CONCLUSIONS: There were significant differences among the different types of gastric polyps in terms of polyp position, shape, and size. The positive rate of HP infection in patients with fundic gland polyps was low. Long-term use of PPIs (>5 years) increased the incidence of fundic gland polyps to some extent. The mechanisms underlying the relationship between gastric polyps, HP infection, and the use of PPIs remain to be further studied.

Ulcerative colitis with acute pleurisy: A case report and review of the literature.

RATIONALE: Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn's disease, are associated with a large number of extraintestinal manifestations. Pulmonary manifestations are infrequently seen in patients with IBD. Moreover, serositis including pleural and pericardial manifestations in UC is rare. PATIENT CONCERNS: We report a case of UC with acute pleurisy in a 43-year-old man; review literature; and discuss the diagnosis, differential diagnosis, and treatment. DIAGNOSES: Active duodenal ulcer was found using gastroscopy. Multiple ulcers in segmented pattern were noticed in the left hemi-colon using colonoscopy. An UC in active stage was confirmed subsequently by histology. INTERVENTION: The patient was treated with bifidobacterium tetravaccine tablets, oral mesalazine and mesalazine enemas. The omeprazole and mucosal protective agents were given to treat the duodenal ulcer. OUTCOMES: As follow-up, the therapy including oral mesalazine and infliximab regularly was continued and the patient condition was stabilized. MAIN LESSON: Pulmonary involvement should be considered in patients who develop pleurisy in UC. Infliximab is considered the better available treatment for patients presenting with pleurisy in UC.

Silibinin inhibits the migration and invasion of human gastric cancer SGC7901 cells by downregulating MMP-2 and MMP-9 expression via the p38MAPK signaling pathway.

The objective of the present study was to observe the effects of silibinin and the p38 mitogen-activated protein kinase (MAPK) signaling pathway inhibitor SB203580 on the migration and invasion capabilities of SGC7901 cells, and to explore the underlying associated mechanisms. Scratch, Transwell and Matrigel invasion assays were performed to study the effects of silibinin on cell migration and invasion. Western blot analysis was used to determine the expression levels of p38MAPK, phosphorylated (p-)p38MAPK, matrix metalloproteinase (MMP)-2 and MMP-9. At the genomic level, quantitative polymerase chain reaction was performed to evaluate the expression levels of MMP-2 and MMP-9. The results of scratch assay indicated that silibinin inhibited the migration capabilities of human gastric cancer SGC7901 cells in a dose-dependent manner. Additionally, Matrigel invasion and Transwell migration assays revealed that silibinin and SB203580 combined treatment significantly reduced the number of invasive cells. Western blot analysis indicated a reduced phosphorylation of p38MAPK without marked changes in p38MAPK expression. In addition, the expression of MMP-2 and MMP-9 significantly decreased in the presence of silibinin, SB203580, and the combination of silibinin and SB203580. In summary, silibinin decreased the invasion and migration abilities of SGC7901 cells by downregulating the expression of MMP-2 and MMP-9 through inhibiting p38MAPK signaling cascades.

Influence of microRNA­34a on proliferation, invasion and metastasis of HCT116 cells.

The aim of the present study was to investigate the role of microRNA (miR)­34a expression in the proliferation, invasion and metastasis of colon cancer and its underlying mechanisms. HCT116 cells were cultured in high­sugar Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum and 1000 U/ml penicillin­streptomycin. Following digestion and resuspension, the cells were used for transfection, expression and western blot analysis. HCT116 cells from miR­34a transfection, negative control and blank control groups were seeded into a 96­well plate at a density of 105 cells/ml, and 200 µl complete DMEM was added. The data are presented as the mean ± standard error. A one­way analysis of variance was performed to compare groups. miR­34a­HCT116 cells demonstrated significantly increased expression levels of miR­34a. The proliferation of HCT116 cells with overexpression of miR­34a was significantly inhibited to 0.49±0.11 compared with the blank control group (P<0.001). Compared with the blank control and negative control groups, the protein expression levels of B­cell lymphoma 2 (Bcl­2) were markedly reduced in the miR­34a transfected group. Furthermore, the protein expression levels of Bcl­2­associated X protein were significantly increased and those of matrix metalloproteinase (MMP)­2 and MMP­9 were markedly reduced in the miR­34a transfected group, MMP­9 to a greater extent. The present study suggested that overexpression of miR­34a may inhibit the proliferation, invasion and metastasis of HCT116 cells.

MiR-34a inhibits colon cancer proliferation and metastasis by inhibiting platelet-derived growth factor receptor α.

The microRNA (miRNA), miR­34a is significant in colon cancer progression. In the present study, the role of miR­34a in colon cancer cell proliferation and metastasis was investigated. It was found that the expression of miR­34a in colon cancer tissues and cell lines was lower when compared with that of normal tissues and cells. Further research demonstrated that miR­34a inhibited cell proliferation, induced G1 phase arrest, and suppressed metastasis and epithelial mesenchymal transition in colon cancer cells. Bioinformatic prediction indicated that platelet­derived growth factor receptor α (PDGFRA) was a potential target gene of miR­34a and a luciferase assay identified that PDGFRA was a novel direct target gene of miR­34a. In addition, assays of western blot analyses and quantitative reverse­transcription polymerase chain reaction confirmed that miR­34a decreased PDGFRA mRNA expression and protein levels in colon cancer cells. Assessment of cellular function indicated that miR­34a inhibited colon cancer progression via PDGFRA. These findings demonstrate that miR­34a may act as a negative regulator in colon cancer by targeting PDGFRA.

Serum microRNA 143 and microRNA 215 as potential biomarkers for the diagnosis of chronic hepatitis and hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies and among the leading causes of cancer death among the whole world. The most urgent needs are to find sensitive markers for early diagnosis or monitor postoperative recurrence and to give adequate treatment for HCC. MicroRNAs (miRNAs) are reported as a group of small non-coding RNAs that can function as endogenous RNA interference to regulate expression of the targeted genes. This study was conducted to detect the application of miR-143 and miR-215 in the diagnosis of HCC. METHODS: A total of 340 serum samples (127 samples from controls, 118 samples from hepatitis and 95 samples from HCC patients) were collected. The levels of the two mature miRNAs (miR-143 and miR-215) were detected by probe-based stem-loop quantitative reverse-transcriptase PCR (RT-qPCR) in controls, hepatitis and HCC patients. Besides, the relationship between miR-143 and miR-215 levels and clinical and pathological factors was explored. RESULTS: We found that the expression of serum miR-215 was distinctly increased in chronic hepatitis compared with controls (mean ± SD: 6.79 ± 0.72 vs. 3.46 ± 0.37, P < 0.001 and mean ± SD: 8.38 ± 0.87 vs. 3.46 ± 0.37, P < 0.001). In addition, we conduct ROC analyses to detect the potential application of miR-143 and miR-215 in the diagnosis of chronic hepatitis and HCC. Our results showed that miR-143 and miR-215 might be a potential biomarker for the hepatitis and HCC. CONCLUSIONS: In conclusion, the expression of miR-143 and miR-215 in serum were significantly up-regulated in patients with chronic hepatitis and HCC. Due to its reasonable sensitivity and specificity for both diseases, miR-143 and miR-215 could be as potential circulating biomarkers. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1048932281272754.

Association of XRCC1 gene polymorphisms with susceptibility to gastric cancer in Chinese Han population.

OBJECTIVES: Gastric cancer is one of the most frequently causing cancer-related deaths worldwide. The X-ray repair complementing group 1 gene (XRCC1) is an important candidate gene for influencing gastric cancer risk. This study aimed to evaluate the associations between XRCC1 genetic variants and gastric cancer susceptibility in Chinese Han population. METHODS: Four hundred twenty-four gastric cancer patients and 430 cancer-free controls were enrolled. Two genetic variants (c.1254C>T and c.1779C>G) of XRCC1 gene were genotyped by created restriction site-polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism methods, respectively. KEY FINDINGS: Results from this study indicated that the allele and genotype frequencies of these two genetic variants were statistically different between gastric cancer patients and cancer-free controls. The association analyses suggested that these two genetic variants were statistically associated with the increased risk of gastric cancer (for c.1254C>T, T versus C: odds ratio (OR) = 1.44, 95% confidence interval (CI) 1.17-1.77; for c.1779C>G, G versus C: OR = 1.51, 95% CI 1.22-1.86). The allele-T of c.1254C>T and allele-G c.1779C>G genetic variants may contribute to the susceptibility to gastric cancer in Chinese Han population. CONCLUSION: Our data suggest that these two genetic variants might be used as molecular markers for evaluating the susceptibility to gastric cancer.