Bioscience reports
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Meta Analysis
Association between the polymorphisms of CALM1 gene and osteoarthritis risk: a meta-analysis based on observational studies.
The existing studies on the association between polymorphisms of Calmodulin 1 (CALM1) gene and the risk of osteoarthritis (OA, a complex multifactorial disease and a major degenerative form of arthritis) in different populations have yielded conflicting findings. Therefore, we conducted a meta-analysis by systematically searching PubMed, Embase, Medline, Cochrane Library and Google Scholar, and assessing this association by calculating pooled odds ratios with 95% confidence intervals. Subgroup analyses stratified by ethnicity, OA type, and genotype were also conducted. ⋯ Stratification analyses by ethnicity and OA type showed that the rs12885713 polymorphism increased the risk of OA among Asians and in knee OA, respectively. In conclusion, the rs12885713 and rs2300496 polymorphisms of the CALM1 gene may both increase the risk of OA. Owing to the limitations of the present study, this finding should be further confirmed in future well-designed studies.
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Background: There is a dispute on the prognostic value of long non-coding RNA regulator of reprogramming (lncRNA ROR) in cancers. The purpose of the present study was to evaluate the prognostic significance of lncRNA ROR expression in human cancers. Methods: PubMed, Embase, and Cochrane Library were searched to look for relevant studies. ⋯ However, there was no significant correlation between lncRNA ROR expression and other CPs, including age (P=0.18), gender (P=0.33), tumor size (P=0.25), or tumor differentiation (P=0.13). Conclusion: High lncRNA ROR expression was associated with worse prognosis in cancers. LncRNA ROR expression could serve as an unfavorable prognostic factor in various cancers.
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MiRNA (miR)-206 plays a tumor suppressor role in various cancer types. Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1). The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively. ⋯ These results could be reversed by the overexpression of TM4SF1. At last, up-regulation of miR-206 suppressed expression of p-AKT and p-ERK by targetting TM4SF1 in PGE2-induced cells. Our results provide further evidence that miR-206 has a protective effect on PGE2-induced colon carcinogenesis.
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Meta Analysis
ERCC1 rs11615 polymorphism increases susceptibility to breast cancer: a meta-analysis of 4547 individuals.
Excision repair cross-complementation group 1 (ERCC1), a DNA repair protein, is vital for maintaining genomic fidelity and integrity. Despite the fact that a mounting body of case-control studies has concentrated on investigating the association of the ERCC1 rs11615 polymorphism and breast cancer risk, there is still no consensus on it. We conducted the current meta-analysis of all eligible articles to reach a much more explicit conclusion on this ambiguous association. ⋯ When excluded, the studies that deviated from Hardy-Weinberg equilibrium (HWE), the pooled results of what remained significantly increase the risk of breast cancer under the allele model (OR = 1.14, 95% CI = 1.02-1.27, P=0.02), heterozygote model (OR = 1.24, 95% CI = 1.06-1.44, P=0.007), and dominant model (OR = 1.21, 95% CI = 1.05-1.41, P=0.01). This increased breast cancer risk was found in Asian population as well as under the heterozygote model (OR = 1.24, 95% CI = 1.05-1.48, P=0.013) and dominant model (OR = 1.20, 95% CI = 1.02-1.42, P=0.03). Our results suggest that the ERCC1 rs11615 polymorphism is associated with breast cancer susceptibility, and in particular, this increased risk of breast cancer existence in Asian population.
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Some patients with intra-abdominal infection (IAI) may develop intra-abdominal hypertension (IAH) during treatment. The present study investigated the impact of IAI combined with IAH on the intestinal mucosal barrier in a rabbit model. Forty-eight New Zealand white rabbits were randomly divided into four groups: (i) IAI and IAH; (ii) IAI alone; (iii) IAH alone; and (iv) Control group. ⋯ IAI combined with IAH aggravates damage of the intestinal mucosal barrier in a rabbit model. The combined effects were significantly more severe compared with a single factor. IAI combined with IAH should be prevented and treated effectively.