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Our previous study demonstrated that the expression of miR-146a-5p was downregulated in non-small cell lung cancer (NSCLC) tissue, which affected the progression and prognosis of patients with NSCLC. Thus, the present study was conducted to investigate the functional mechanism of miR-146a-5p in tumorigenesis and angiogenesis in NSCLC. Following the construction of a H460 NSCLC cell line in which miR-146a-5p was overexpressed via lentivirus transduction, the NSCLC chick embryo chorioallantoic membrane (CAM) model was established by transplanting miR-146a-5p-overexpressing NSCLC cells into the CAM. Then, the size of the neoplasms within the CAM was measured, the vessel ratio was calculated, and the cellular morphology, metastasis and inflammation of tumor cell was observed using hematoxylin and eosin staining. The target genes of miR-146a-5p were predicted by 12 online software programs; these genes were then subjected to Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway annotations using the Database for Annotation, Visualization and Integrated Discovery 6.7 as well as constructed into a protein interaction network using protein-protein interaction from Search Tool for the Retrieval of Interacting Genes/Proteins. The xenograft tumor size and angiogenesis conditions of the miR-146a-5p-overexpressing group (volume 6.340±0.066 mm³, vessel ratio 9.326±0.083) was obviously restricted (P<0.001) when compared with the low expression group (volume 30.13±0.06 mm³, vessel ratio 16.94±0.11). In addition, marked necrosis along with inflammatory cell infiltration was observed with the HE-stained slices from the miR-146a-5p low expression group. Regarding the results of the target gene prediction, cancer and toll-like receptor signaling were the two most significant pathways represented among the target genes, while JUN, EGFR and RAC1 were the most relevant proteins among the selected potential targets of miR-146a-5p. In a CAM xenograft tumor model, overexpression of miR-146a-5p inhibited the tumorigenesis and angiogenesis of an NSCLC cell line. miR-146a-5p may act as a tumor suppressor gene in NSCLC and have moderate prognostic value in lung cancer. [ABSTRACT FROM AUTHOR]

Intrahepatic cholangiocarcinoma (ICC) arises from the biliary epithelium and is a relatively rare and highly fatal neoplasm. The prognosis is poor, and survival is limited to a few months. Here, we report a case of advanced ICC that was successfully treated with apatinib, a new oral tyrosine kinase inhibitor that targets the intracellular domain of vascular endothelial growth factor receptor-2. To the best of our knowledge, this is the first case report of the successful use of apatinib for advanced ICC; this treatment has demonstrated fewer toxic effects than traditional cytotoxic chemotherapy. The progression-free survival time was 8 months. The only toxicity observed was mild hand–foot syndrome. Therefore, apatinib may be an additional option for the treatment of advanced ICC, but further prospective studies are needed to optimize the treatment. [ABSTRACT FROM AUTHOR]

Background: Non-small cell lung cancer (NSCLC) has led to the highest cancer-related mortality for decades. To enhance the efficiency of early diagnosis and therapy, more efforts are urgently needed to reveal the origins of NSCLC. In this study, we explored the effect of miR-542-5p in NSCLC with clinical samples and in vivo models and further explored the prospective function of miR-542-5p though bioinformatics methods.Methods: A total of 125 NSCLC tissue samples were collected, and the expression of miR-542-5p was detected by qRT-PCR. The relationship between miR-542-5p level and clinicopathological features was analyzed. The effect of miR-542-5p on survival time was also explored with K-M survival curves and Cox's regression. The effect of miR-542-5p on the tumorigenesis of NSCLC was verified with a chick chorioallantoic membrane (CAM) model. The potential target genes were predicted by bioinformatics tools, and relevant pathways were analyzed by GO and KEGG. Several hub genes were validated by Proteinatlas.Results: The expression of miR-542-5p was down-regulated in NSCLC tissues, and consistent results were also found in the subgroups of adenocarcinoma and squamous cell carcinoma. Down-regulation of miR-542-5p was found to be connected with advanced TNM stage, vascular invasion, lymphatic metastasis and EGFR. Survival analyses showed that patients with lower miR-542-5p levels had markedly poorer prognosis. Both tumor growth and angiogenesis were significantly suppressed by miR-542-5p mimic in the CAM model. The potential 457 target genes of miR-542-5p were enriched in several key cancer-related pathways, such as morphine addiction and the cAMP signaling pathway from KEGG. Interestingly, six genes (GABBR1, PDE4B, PDE4C, ADCY6, ADCY1 and GIPR) from the cAMP signaling pathway were confirmed to be overexpressed in NSCLCs tissues.Conclusions: This evidence suggests that miR-542-5p is a potential tumor-suppressed miRNA in NSCLC, which has the potential to act as a diagnostic and therapeutic target of NSCLC. [ABSTRACT FROM AUTHOR]

It has been discovered that miR-133a-3p acts as a tumor suppressor in bladder cancer (BC). Nevertheless, the function of miR-133a-3p in BC remains unclarified. Thus, we carried out this study to validate the expression of miR-133a-3p in BC and provide insights into the molecular mechanism underlying it. To assess the expression of miR-133a-3p in BC, we searched eligible studies from literature and Gene expression Omnibus (GEO) to perform a meta-analysis. We also plotted the summary receiver operating characteristic (SROC) curve to evaluate the diagnostic ability of miR-133a-3p in BC. Additionally, the potential target genes of miR-133a-3p were acquired from 14 online software programs and GEO database. Protein-protein interaction (PPI) network was created to identify the hub genes. Then, Gene Ontology (GO) functional annotation analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were carried out to investigate the regulatory network of the target genes. From the meta-analysis, miR-133a-3p was remarkably downregulated in BC tissues compared with that in non-cancer tissues (standard mean difference =-3.84, 95% confidence interval =-6.99-0.29). Moreover, results from SROC suggested that miR-133a-3p exhibited the ability to diagnose BC (area under curve =0.8418). As for the bioinformatics study, 488 genes were chosen as the potential targets of miR-133a-3p in BC, among which 10 genes were defined as hub genes (all degrees >5). Further GO and KEGG pathway analysis indicated that the target genes of miR-133a-3p aggregated in specific biological process and pathways. In conclusion, miR-133a-3p possessed great diagnostic potential with its downregulation in BC, and miR-133a-3p might serve as a novel biomarker for BC. [ABSTRACT FROM AUTHOR]

Wound healing is a dynamic and complex biologic process that could be accelerated by growth factors. To investigate the efficacy of topical recombinant human acidic fibroblast growth factor (rh-aFGF) treatment in deep partial-thickness burn or skin graft donor sites, we designed a randomized, multicenter, double-blind, and placebo-controlled clinical trial. The healing rate, fully healed rate, and healing time were evaluated to assess the efficacy of rh-aFGF application. Laboratory examinations and abnormal signs were used to assess the side and toxic effects. The results showed that the healing rate of burn wounds and skin graft donor sites treated by rh-aFGF was significantly higher than that by placebo, and the mean healed time of burn wounds and skin graft donor sites in the rh-aFGF group was significantly the shorter than that in the placebo group. In conclusion, topical administration of rh-aFGF can accelerate the wound healing process and shorten the healed time. It is a potential therapeutic application for promoting healing of deep partial-thickness burns or skin graft donor sites. [ABSTRACT FROM AUTHOR]

A single nucleotide polymorphism, −160C→A, has been identified in the promoter region of the E-cadherin gene and has been shown to alter its transcriptional activity. To assess susceptibility of −160A allele carriers to seven types of cancers, the authors conducted a comprehensive meta-analysis, up to November 2006, of 26 case-control studies comprising 7,042 cases and 7,011 controls. Pooled odds ratios and 95% confidence intervals were calculated by using the random-effects model. Publication bias, subgroup, and sensitivity analyses were also performed, which showed that −160A allele carriers, compared with noncarriers, had about a 17–19% increased risk of several invasive/metastatic tumors. Analyses of various types of cancers revealed that, in Europeans, the −160AA homozygote was associated with an increased risk of urothelial cancer, carriers of −160A were at increased risk of lung and prostate cancers, and carriers of −160A with gastric cancer were found to suffer a significantly increased risk, whereas their Asian counterparts seemed to be tolerant. No evidence was found that the −160A allele predisposed its carriers to breast, colorectal, or esophageal cancers. These findings indicate that −160A of the E-cadherin gene is emerging as a low-penetrance tumor susceptibility allele for the development of gastric, lung, prostate, and urothelial cancers. [ABSTRACT FROM AUTHOR]