The objective of this study was to investigate the expression, proliferation, and apoptosis function of long-chain non-coding RNA maternally expressed gene 3 (MEG3) and antisense non-coding RNA at the INK4 locus (ANRIL) in gallbladder cancer (GBC) tissues. GBC tissues and adjacent normal samples were collected from 84 patients from January 2008 to June 2010. Empty vector, pcDNA-MEG3, and pcDNA-ANRIL vectors were transfected into GBC-SD and QBC939 cells. An MTT assay, real-time quantitative polymerase chain reaction (RT-qPCR), flow cytometry, Western blotting, and immunohistochemistry were applied. The effects of MEG3 and ANRIL were also verified in mice. Compared with normal tissues, the expression of MEG3 was significantly lower in GBC tissues, whereas the expression of ANRIL was significantly higher (both P < 0.05). The overexpression of MEG3 and underexpression of ANRIL were significantly associated with GBC prognosis (both P < 0.05). The expressions of MEG3 and ANRIL were higher in pcDNA-MEG3 and pcDNA-ANRIL-transfected cells than in empty vector-transfected cells in vitro (both P < 0.05). Most of the pcDNA-MEG3-transfected cells were in the G0-G1 phase, which showed reduced cell activity and clone counts and increased p53 and decreased cyclin D1, whereas the pcDNA-ANRIL-transfected cells were mostly in the S phase and showed contrasting behavior. Mice injected with pcDNA-MEG3-transfected cells had smaller and lighter tumors, decreased ki-67 levels, and increased caspase 3 levels, whereas those injected with pcDNA-ANRIL showed contrasting results (all P < 0.05). MEG3 can inhibit the proliferation of GBC cells and promote apoptosis, whereas ANRIL can improve the proliferation of gallbladder cells and inhibit apoptosis. Collectively, our results suggest that therapeutic strategies directed toward upregulating MEG3 and downregulating ANRIL may be clinically relevant for the inhibition of GBC deterioration.

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BackgroundRecent studies implicate adipokines in the pathogenesis of inflammatory diseases, including psoriasis. In this study we evaluated the significance of serum resistin levels in psoriasis patients using a meta-analysis approach.223MethodsRelevant articles were retrieved by searching the following English and Chinese databases: Cochrane Library, PubMed, Springer Link, Chinese Biomedical Database (CBM) and Chinese National Knowledge Infrastructure (CNKI). The retrieved studies were subjected to a thorough screening procedure to identify case–control studies that contained the required data. Data was extracted from each study and Version 12.0 STATA statistical software was employed for statistical analyses.ResultsNine case–control studies, containing 421 psoriasis patients and 348 healthy controls, were included in this study. The major result of the meta-analysis revealed a statistically significant association between serum resistin levels and psoriasis (SMD = 2.22, 95%CI: 1.14-3.29, P < 0.001). Subgroup analysis based on ethnicity showed that, compared to the healthy controls, serum resistin levels were markedly higher in psoriasis patients in both Asian and Caucasian populations (Asians: SMD = 3.27, 95%CI = 1.62 ~ 4.91, P < 0.001; Caucasians: SMD = 0.91, 95%CI = 0.28 ~ 1.54, P < 0.001).ConclusionsBased on our results, we conclude that serum resistin level in psoriasis patients is higher than healthy controls, and raises the possibility that elevated serum resistin levels may be a novel diagnostic marker in psoriasis and may predict the occurrence of co-morbidities in psoriasis patients.

Background: Gastric cancer (GC) is a common cause of cancer-related mortality worldwide, and microRNAs (miRNAs) have been shown to play an important role in GC development. This study aims to explore the effect of microRNA-93-5p (miR-93-5p) on the epithelial-mesenchymal transition (EMT) in GC, via AHNAK and the Wnt signaling pathway. Methods: Microarray-based gene expression analysis was performed to identify GC-related differentially expressed miRNAs and genes. Then the expression of the miR-93-5p was examined in GC tissues and GC cell lines. The targeting relationship between miR-93-5p and AHNAK was verified by a dual luciferase reporter gene assay. In an attempt to ascertain the contributory role of miR-93-5p in GC, miR-93-5p mimic or inhibitor, as well as an AHNAK overexpression vector, were introduced to HGC-27 cells. HGC-27 cell migration and invasive ability, and EMT were assayed using Transwell assay and western blot analysis. Regulation of the Wnt signaling pathway was also assessed using TOP/FOP flash luciferase assay. Results: miR-93-5p was highly expressed in GC tissue samples and cells. Notably, miR-93-5p could target and negatively regulate AHNAK. Down-regulation of miR-93-5p or overexpression of AHNAK could suppress the migration and invasion abilities, in addition to EMT in GC cells via inactivation of the Wnt signaling pathway. Conclusion: Taken together, downregulation of miR-93-5p attenuated GC development via the Wnt signaling pathway by targeting AHNAK. These findings provide an enhanced understanding of miR-93-5p as a therapeutic target for GC treatment.

RIG‐I is associated with the occurrence and development of many tumors. However, the role of RIG‐I in radiotherapy and chemotherapy in NPC has not been reported to date. In our study, RIG‐I expression was significantly reduced in chemoradiotherapy‐resistant NPC tissues and cells compared with that in therapy‐sensitive tissues and cells. RIG‐I expression increased in nonresistant NPC cells, including CNE1 and CNE2, in a dose‐dependent manner with increasing chemotherapy drug concentration or radiotherapy dose. RIG‐I overexpression promoted radiotherapy and chemotherapy sensitivity in NPC cells, leading to cellular apoptosis and increased expression of the proapoptotic factors BAX and caspase‐3. Similarly, RIG‐I knockdown in NPC cells promoted chemoradiotherapy resistance and reduced apoptosis. Analysis of microarray data indicated that the expression of IFN/JAK2 and endoplasmic reticulum (ER) stress response markers, such as JAK2, STAT1, IRF9, IFNB1, IRF3, p‐IRF3, XBP1, ATF6, IFIT2, and ISG15, was inhibited in chemoradiotherapy‐resistant cells compared with that in sensitive cells. Conversely, activation of IFN/JAK2 and ER stress response pathways in NPC cells reduced paclitaxel resistance and increased apoptosis. RIG‐I promotes IFN/JAK2 and ER stress response‐mediated apoptosis to inhibit chemoradiation resistance in nasopharyngeal carcinoma.

Background: Esophageal cancer (EC) is one of the most common malignant tumors of the digestive system. MiR-25-3p was proved to be a biomarker for the diagnosis and treatment of many cancers. MiR-25-3p was found to be high expressed in the blood of EC patients. The aim of this study was to explore the effect of miR-25-3p and its target gene on EC. Methods: miR-25-3p expression in the blood of EC patients and EC cells was detected by RT-qPCR. The target of miR-25-3p was identified by bioinformatics and luciferase reporter assay. After transfection, cell viability, apoptosis, migration and invasion were detected by MTT, flow cytometry, wound healing and transwell assays, respectively. The expressions of PTEN, Bax, Bcl-2, cleaved Caspase-3, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blot. Results: MiR-25-3p was high expressed in the blood of EC patients and EC cells. MiR-25-3p targeted PTEN and inhibited the expression of PTEN. MiR-25-3p mimic increased the viability, migration, invasion and the expressions of Bcl-2 and Cleaved caspase-3, and inhibited the apoptosis and the expression of Bax in EC cells. MiR-25-3p mimic also enhanced the expressions of p-PI3K and p-AKT and the ratios of p-PI3K/PI3K and p-AKT/AKT in EC cells. PTEN overexpression not only had an opposite effect of miR-25-3p mimic, but also reversed the effect of miR-25-3p mimic on EC cells. Conclusion: MiR-25-3p targeted PTEN to promote the migration and invasion, and inhibit apoptosis of EC cells via the PI3K/AKT pathway, which might provide a new therapeutic target for EC treatment.

The clear cell renal cell carcinoma (ccRCC) is the main pathological subtype of renal cell carcinoma. Immune system evasion, one hallmark of cancer, contributes to cancer cells in escaping from the attack of immune cells. In order to identify potential prognostic biomarkers in ccRCC patients and immune cells fraction, we collected and downloaded profiles from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database. We obtained 2 modules significantly associated with tumor stage and immune cells; functional enrichment analysis showed that genes in the module ‘yellow’ were significantly enriched in proteins targeting to membrane and ribosome, as well as the oxidative phosphorylation pathway, while genes in the module ‘green’ mainly participate in molecular functions associated with immunity like activation of T cells. Four LncRNAs ( LINC00472, AL590094.1, AL365203.3 , and AC147651.3 ) and RPL27A and RPL22L1 in the module ‘yellow’ and two lncRNAs ( LINC00426 and AC129507.2 ) and five protein-coding genes ( CSF1, NOD2, ITGAE, CD7 , and PDCD1 ) in the module ‘green’ represented independent prognostic values in patients with ccRCC. Expression of LINC0042, NOD2, CD7 , and PDCD1 were significantly correlated with ratio of immune cells (like T cells CD8 and resting mast cells). LINC00426 , with significant correlation with immune cell fraction, shows potential prognostic value in ccRCC patients. Our findings provide a strategy in exploring biomarkers with prognostic significance and significant association with the fraction of immune cells.

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