BackgroundFew long noncoding RNAs (lncRNAs) that act as oncogenic genes in breast cancer have been identified.MethodsOncogenic lncRNAs associated with tumourigenesis and worse survival outcomes were examined and validated in Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), respectively. Then, the potential biological functions and expression regulation of these lncRNAs were studied via bioinformatics and genome data analysis. Moreover, progressive breast cancer subtype-specific lncRNAs were investigated via high-throughput sequencing in our cohort and TCGA validation. To elucidate the mechanisms of the regulation of these lncRNAs, genomic alterations from the TCGA, Broad, Sanger and BCCRC data, as well as epigenetic modifications from GEO data, were then applied and examined to meet this objective. Finally, cell proliferation assays, flow cytometry analyses and TUNEL assays were applied to validate the oncogenic roles of these lncRNAs in vitro.ResultsA cluster of oncogenic lncRNAs that was upregulated in breast cancer tissue and was associated with worse survival outcomes was identified. These oncogenic lncRNAs are involved in regulating immune system activation and the TGF-beta and Jak-STAT signalling pathways. Moreover, TINCR, LINC00511, and PPP1R26-AS1 were identified as subtype-specific lncRNAs associated with HER-2, triple-negative and luminal B subtypes of breast cancer, respectively. The up-regulation of these oncogenic lncRNAs is mainly caused by gene amplification in the genome in breast cancer and other solid tumours. Finally, the knockdown of TINCR, DSCAM-AS1 or HOTAIR inhibited breast cancer cell proliferation, increased apoptosis and inhibited cell cycle progression in vitro.ConclusionsThese findings enhance the landscape of known oncogenic lncRNAs in breast cancer and provide insights into their roles. This understanding may potentially aid in the comprehensive management of breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0696-6) contains supplementary material, which is available to authorized users.

Solar energy can be used as “green” energy by photocatalysis for the nitrogen fixation under the atmospheric conditions compared with the traditional energy-intensive industrial production of ammonia. However, the complex kinetics and high reaction barriers greatly hinder the development of the photocatalytic N2 reduction reaction. Herein, a BiOBr/MXene-Ti3C2 composite catalyst is prepared by the simple electrostatic adsorption and self-assembly method. The as-prepared 10 wt % BiOBr/Ti3C2 exhibits the best performance for N2 fixation to NH3 by photocatalysis. The evolution rate of NH3 is up to 234.6 μmol·g–1·h–1, which is approximately 48.8 times and 52.4 times higher than those of pure BiOBr and Ti3C2, respectively. It is found that the designed double vacancies of oxygen and titanium for BiOBr/Ti3C2 composites, with the availability of localized electrons, have the ability to adsorb and activate N2, which can be efficiently reduced to NH3 by the interfacial electrons transferred from the excited BiOBr/Ti3C2 composite. In addition, the results of in situ Fourier transform infrared show the generation of N x H y species by the continuous protonation processes. Moreover, titanium vacancy (VTi) induces a strong absorption energy for nitrogen atoms on the surface of BiOBr/Ti3C2 according to the density functional theory calculations. In particular, the P-electron feedback caused by VTi could effectively promote the weakening of the NN triple bond and elongate the N2 bond length by ∼31.6%. This work might provide new insights into the synergistic effect of double defects and inspiration for the rational design of catalysts by defect engineering in the field of catalytic synthesis of ammonia.

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