Long non-coding RNAs (lincRNAs), a relatively recently recognized class of widely transcribed genes, are thought to affect chromatin state and epigenetic regulation, but their mechanisms of action and potential roles in human disease are poorly understood. This study shows that long non-coding RNAs in the human HOX loci are systematically dysregulated during breast cancer progression, and that expression levels of the lincRNA termed HOTAIR can predict cancer metastasis. Elevated levels of HOTAIR can lead to altered patterns of Polycomb binding to the genome. These findings indicate that lincRNAs have active roles in modulating the cancer epigenome and may be important targets for cancer diagnosis and therapy. Large intervening non-coding RNAs (lincRNAs) are pervasively transcribed in the genome. Here it is shown that lincRNAs in the HOX genetic loci are dysregulated during breast cancer progression in human cells, and that expression levels of the lincRNA called HOTAIR can predict whether a tumour will metastasize. Moreover, enforced expression of HOTAIR can lead to altered patterns of binding of the PRC2 protein to the genome. Large intervening non-coding RNAs (lincRNAs) are pervasively transcribed in the genome1,2,3 yet their potential involvement in human disease is not well understood4,5. Recent studies of dosage compensation, imprinting, and homeotic gene expression suggest that individual lincRNAs can function as the interface between DNA and specific chromatin remodelling activities6,7,8. Here we show that lincRNAs in the HOX loci become systematically dysregulated during breast cancer progression. The lincRNA termed HOTAIR is increased in expression in primary breast tumours and metastases, and HOTAIR expression level in primary tumours is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb repressive complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. Conversely, loss of HOTAIR can inhibit cancer invasiveness, particularly in cells that possess excessive PRC2 activity. These findings indicate that lincRNAs have active roles in modulating the cancer epigenome and may be important targets for cancer diagnosis and therapy.

In recent years, Carbon Capture and Storage (Sequestration) (CCS) has been proposed as a potential method to allow the continued use of fossil-fuelled power stations whilst preventing emissions of CO₂ from reaching the atmosphere. Gas, coal (and biomass)-fired power stations can respond to changes in demand more readily than many other sources of electricity production, hence the importance of retaining them as an option in the energy mix. Here, we review the leading CO₂ capture technologies, available in the short and long term, and their technological maturity, before discussing CO₂ transport and storage. Current pilot plants and demonstrations are highlighted, as is the importance of optimising the CCS system as a whole. Other topics briefly discussed include the viability of both the capture of CO₂ from the air and CO₂ reutilisation as climate change mitigation strategies. Finally, we discuss the economic and legal aspects of CCS.

In this paper, three of the leading options for large scale CO₂ capture are reviewed from a technical perspective. We consider solvent-based chemisorption techniques, carbonate looping technology, and the so-called oxyfuel process. For each technology option, we give an overview of the technology, listing advantages and disadvantages. Subsequently, a discussion of the level of technological maturity is presented, and we conclude by identifying current gaps in knowledge and suggest areas with significant scope for future work. We then discuss the suitability of using ionic liquids as novel, environmentally benign solvents with which to capture CO₂. In addition, we consider alternatives to simply sequestering CO₂—we present a discussion on the possibility of recycling captured CO₂ and exploiting it as a C₁ building block for the sustainable manufacture of polymers, fine chemicals, and liquid fuels. Finally, we present a discussion of relevant systems engineering methodologies in carbon capture system design.

David Wong, Howard Chang and colleagues report the identification of long noncoding RNAs transcribed from the promoters of cell cycle genes. Many of these RNAs have periodic expression during the cell cycle and are regulated by oncogenic stimuli, stem cell differentiation or DNA damage. Transcription of long noncoding RNAs (lncRNAs) within gene regulatory elements can modulate gene activity in response to external stimuli, but the scope and functions of such activity are not known. Here we use an ultrahigh-density array that tiles the promoters of 56 cell-cycle genes to interrogate 108 samples representing diverse perturbations. We identify 216 transcribed regions that encode putative lncRNAs, many with RT-PCR–validated periodic expression during the cell cycle, show altered expression in human cancers and are regulated in expression by specific oncogenic stimuli, stem cell differentiation or DNA damage. DNA damage induces five lncRNAs from the CDKN1A promoter, and one such lncRNA, named PANDA, is induced in a p53-dependent manner. PANDA interacts with the transcription factor NF-YA to limit expression of pro-apoptotic genes; PANDA depletion markedly sensitized human fibroblasts to apoptosis by doxorubicin. These findings suggest potentially widespread roles for promoter lncRNAs in cell-growth control.