The noncoding components of the genome, including miRNA, can contribute to pathogenesis of gastric cancer. Their expression has been profiled in many human cancers, but there are a few published studies in gastric cancer. It is necessary to identify novel aberrantly expressed miRNAs in gastric cancer. In this study, the expression profile of 1891 miRNAs was analyzed using a miRCURY array LNA miRNA chip from three gastric cancer tissues and three normal tissues. The expression levels of 4 miRNAs were compared by real-time PCR between cancerous and normal tissues. We found that 31 miRNAs are upregulated in gastric cancer (P < 0.05) and 10 miRNAs have never been reported by other studies; 30 miRNA are downregulated (P < 0.05) in gastric cancer tissues. Gene ontology analysis revealed that those dysregulated miRNAs mainly take part in regulating cell proliferation. The levels of has-miR-105, -213∗, -514b, and -548n were tested by real-time PCR and have high levels in cancerous tissues. Here, we report a miRNA profile of gastric cancer and provide new perspective to understand this malignant disease. This novel information suggests the potential roles of these miRNAs in the diagnosis, prognosis biomarkers, or therapy targets of gastric cancer.

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ABSTRACT. We aimed to assess the role of polymorphisms of the XRCC1 Arg194Trp, XRCC1 Arg399Gln, ERCC5 His1104Asp, and ERCC5 His46His genes on clinical outcomes of advanced non-small cell lung cancer (NSCLC) patients receiving platinum-based chemotherapy regimens. A total of 378 NSCLC patients were asked to participate within 1 month after diagnosis between January 2005 and January 2006, and they were followed up until November 2011. Genomic DNA of the four genes was extracted using the Qiagen Blood Kit. Results showed that individuals with XRCC1 399A/A and ERCC5 46T/T genotypes were more likely to show positive responses to chemotherapy, with odds ratio (OR) = 2.27 and 95% confidence interval (CI) = 1.64-6.97, and OR = 1.90, CI = 1.10-3.28, respectively. The XRCC1 399A/A genotype was significantly associated with longer progression-free survival (PFS) and overall survival (OS) rates, and the hazard ratios (HRs) (95%CI) were 0.48 (0.25-0.88) and 0.51 (0.26-0.98), respectively. Similarly, NSCLC patients carrying the ERCC5 46T/T genotype were more likely to show increased PFS and OS, with HRs (95%CI) of 0.47 (0.22-0.82) and 0.52 (0.31-0.96), respectively. In conclusion, our study indicated that XRCC1 Association of XRCC1 and ERCC5 with NSCLC Arg399Gln and ERCC5 His46His might significantly influence the response to chemotherapy, and the two genetic polymorphisms are suggested to be routinely detected to determine NSCLC patients that are more likely to benefit from chemotherapy.

ABSTRACT. Individual differences in chemosensitivity and clinical outcome of non-small-cell lung carcinoma (NSCLC) patients can be influenced by host-inherited factors. We investigated the impact of XRCC1 Arg194Trp, XRCC1 Arg280His, XRCC1 Arg399Gln, XPD Arg156Arg, XPD Asp312Asn, XPD Asp711Asp, and XPD Lys751Gln gene polymorphisms on treatment efficacy in 375 NSCLC patients on platinum-based chemotherapy. We also examined progressionfree survival and overall survival. The gene polymorphisms were analyzed by duplex PCR. The patients with XRCC1 399A/A had a significantly better response to chemotherapy. Individuals with XPD 711 Asp and XPD 312 Asn alleles responded poorly to chemotherapy when compared with the wide-type genotype. The adjusted hazard ratio DNA repair gene and NSCLC prognosis (HR) in the Cox regression model was calculated. The XRCC1 399A/A polymorphism was associated with better progression free survival and overall survival of NSCLC patients (HR=0.61 and 0.55). On the other hand, the XPD 711 Asp allele was associated with poorer progression free survival and overall survival compared to the C/C genotype, with HRs of 1.89 and 1.90. The XPD 312 Asn allele was found to be associated with non-significantly reduced survival of NSCLC patients (HR = 1.73). In conclusion, we found the polymorphisms of XRCC1 and XPD to be related to the efficacy of platinum-based chemotherapy in NSCLC patients. This information should aid in therapeutic decisions for individualized therapy in NSCLC cases.

Recently, the development of novel metal-containing resists has received much attention in extreme ultraviolet lithography (EUVL) owing to their smaller sizes and higher EUV absorptivity than traditional polymer resists. Herein,...

Increasing evidence has demonstrated that cell adhesion molecule 1/tumor suppressor in lung cancer 1 (CADM1/TSLC1) is crucially implicated in various biological processes, including proliferation, apoptosis, and invasion during tumorigenesis and development. However, the mechanism underlying its suppression of tumor growth and metastasis in melanoma remains elusive. The aim of the present study was to examine if CADM1/TSLC1 was able to induce growth suppression in melanoma. The plasmid pcDNA3.1‑CADM1/TSLC1 was transfected into A375 cells (a human melanoma cell line). The expression of CADM1/TSLC1 in the transfected cells was determined by RT‑PCR and western blotting analysis. Cell growth was measured by an 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyl‑tetrazolium bromide assay and cell apoptosis was determined by flow cytometry, while a transwell assay was utilized to measure the ability of invasion. The expression of MMP‑2 and MMP‑9 in the transfected cells was determined by western blotting analysis. RT‑PCR and western blotting revealed that in pcDNA3.1‑CADM1/TSLC1 the protein expression of CADM1/TSLC1 protein was higher than in the pcDNA3.1 and A375 cells. The expression of MMP‑2 and MMP‑9 was lower in the pcDNA3.1‑CADM1/TSLC1 than that in the pcDNA3.1 and A375 cells. The growth of CADM1/TSLC1‑transfected cells was significantly suppressed in vitro and the ability of invasion was also reduced, CADM1/TSLC1 was able to induce cell apoptosis. Furthermore, CADM1/TSLC1 was an anti‑invasive gene, the overexpression of which inhibited the invasion of A375 cells. This inhibition may be due to the suppression of the MMP‑2 and MMP‑9 expression, which is relative to tumor metastasis and progression.

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