BackgroundColorectal cancer (CRC) was one of the most commonly diagnosed malignancies. The molecular mechanisms involved in the progression of CRC remain unclear. Accumulating evidences showed that long noncoding RNAs (lncRNAs) played key roles in tumorigenesis, cancer progression, and metastasis. Therefore, we aimed to explore the roles of lncRNAs in the progression of CRC.MethodsIn this study, we aimed to identify differentially expressed lncRNAs and messenger RNAs (mRNAs) in CRC by analyzing a cohort of previously published datasets: GSE64857. GO and KEGG pathway analyses were applied to give us insight in the functions of those lncRNAs and mRNAs in CRC.ResultsTotally, 46 lncRNAs were identified as differentially expressed between stage II and stage III CRC for the first time screening by microarray. GO and KEGG pathway analyses showed that differentially expressed lncRNAs were involved in regulating signal transduction, cell adhesion, cell differentiation, focal adhesion, and cell adhesion molecules.ConclusionsWe found three lncRNAs (LOC100129973, PGM5-AS1, and TTTY10) widely co-expressed with differentially expressed mRNAs. We also constructed lncRNA-associated PPI in CRC and found that these lncRNAs may be associated with CRC progression. Moreover, we found that high PGM5-AS1 expression levels were associated with worse overall survival in CRC cancer. We believe that this study would provide novel potential therapeutic and prognostic targets for CRC.Electronic supplementary materialThe online version of this article (doi:10.1186/s12957-017-1211-7) contains supplementary material, which is available to authorized users.

Introduction: Hodgkin lymphoma (HL) is a type of lymphoma common throughout the western countries. However, the detailed mechanisms and special biomarkers of HL remain to be further investigated. Emerging studies have shown that long non-coding RNAs play a key role in human cancers. Material and methods: In the present work, we constructed relapse-related lncRNA-mediated ceRNA networks in HL. Additionally, we constructed co-expression networks for these relapse-related lncRNAs. We also constructed a relapse-related lncRNA-miRNA-mRNA network to study the potential mechanism of these lncRNAs. Furthermore, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to explore functions of DEGs in Hodgkin lymphoma. Results: A total of 18 lncRNAs were found to be dysregulated between early relapse and late relapse HL. Six lncRNAs (PCBP1-AS1, HCG18, GAS5, PSMD6-AS2, PRKCQ-AS1, SNHG6), 116 mRNAs and 121 miRNAs were included in the ceRNA network. Bioinformatics analyses revealed that these lncRNAs were significantly involved in regulating immune system processes, responses to chemical stimuli and responses to stress. Among them, HCG18 and PCBP1-AS1 were identified as key lncRNAs in HL relapse. Conclusions: Our results for the first time constructed the key relapse-related lncRNA-mediated ceRNA networks in Hodgkin lymphoma progression. We trust that this work will provide a new therapeutic and prognostic target for HL.

miR‐145 has been found to be significantly downregulated in gliomas, and overexpression of miR‐145 increases glioma cell apoptosis and enhances chemosensitivity or herpes simplex virus thymidine kinase gene therapy. However, the correlation between miR‐145 and the clinical prognosis of glioblastomas has never been explored. In this study, a retrospective study was conducted in 86 cases of patients with glioblastoma after neurosurgery combined with chemoradiotherapy, and 36 cases with traumatic brain injury. Our results showed that miR‐145 was significantly lower in glioblastoma tissues than that in normal brain tissue (P < 0.05). Furthermore, miR‐145 was lower in patients with lower Karnofsky Performance Scale (KPS) scores than in patients with higher KPS scores ( P < 0.05). Cox Regression analysis showed that low miR‐145 expression was associated with poor patient survival ( P < 0.05). These data suggested that patients with glioblastoma with lower miR‐145 expression are prone to shorter overall survival.

In pursuit of a novel approach in breast cancer therapy, we explored the ability of vanadium-rutin complex to eradicate cancer by efficiently targeting various apoptotic pathways on human breast cancer cell lines. We provide direct proof of the chemotherapeutic potential of the vanadium-rutin complex by activating p-53 dependent intrinsic apoptosis and modulating the VEGF pathways. The complex was also capable of binding and cleaving CT-DNA at different concentrations. The complex was able to inhibit cell viability at 100 and 150 µM doses in both MCF7 and MDA-MB-231 cells. Furthermore, the complex successfully initiated apoptosis in both cell lines by activating the p53 dependent intrinsic apoptotic pathway. In vitro studies also established that the complex modulated p53, Bax, Bcl2 and VEGF expressions and induced DNA fragmentation in both the cell lines.