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In the last years power computing and communication technologies have improved greatly, while at the same time immersive and wearable user interfaces became available at a consumer level. The widespread of these technologies fostered research in the field of telexistence and robot avatars, making it mature enough to be deployed out of the lab. There is a general consensus that enabling the remotization of physical activities would have a large impact on both safety and effciency of industrial processes. In this paper we report our work towards the development of robot avatars for industrial applications and the preliminary results of their deployment in real use cases.

The original version of this Article omitted a declaration from the competing interests statement, which should have included the following: ‘One of the authors, Y.L., is an editor on the staff of Nature Communications, but was not in any way involved in the journal review process. The other authors declare no competing interests’. This has now been corrected in both the PDF and HTML versions of the Article.

MicroRNA 26a (miR-26a) reduces cell viability in several cancers, indicating that miR-26a could be used as a therapeutic option in patients. We demonstrate that miR-26a not only inhibits G1-S cell cycle transition and promotes apoptosis, as previously described, but also regulates multiple cell cycle checkpoints. We show that sustained miR-26a over-expression in both breast cancer (BC) cell lines and mouse embryonic fibroblasts (MEFs) induces oversized cells containing either a single-large nucleus or two nuclei, indicating defects in mitosis and cytokinesis. Additionally, we demonstrate that miR-26a induces aneuploidy and centrosome defects and enhances tumorigenesis. Mechanistically, it acts by targeting G1-S transition genes as well as genes involved in mitosis and cytokinesis such as CHFR, LARP1 and YWHAE. Importantly, we show that only the re-expression of CHFR in miR-26a over-expressing cells partially rescues normal mitosis and impairs the tumorigenesis exerted by miR-26a, indicating that CHFR represents an important miR-26a target in the regulation of such phenotypes. We propose that miR-26a delivery might not be a viable therapeutic strategy due to the potential deleterious oncogenic activity of this miRNA.

Prostate cancer is the most frequently diagnosed malignancy among men in the Western world. The development and growth of prostate cancer is dependent upon androgens, whose effects are mediated by the androgen receptor (AR), a member of the nuclear receptor superfamily of ligand-activated transcription factors. The identification of androgen-regulated genes in prostate cancer cells, particularly those involved in cell growth, cell survival and cell migration are, therefore, of great importance for defining the mechanisms of prostate cancer development and progression, and thus developing new markers and targets for prostate cancer treatment. Our laboratory has previously carried out gene expression microarray analysis using the androgen-responsive LNCaP prostate cancer cell line, to identify androgen-regulated genes. Amongst the most highly androgen-responsive genes was Glycine N-methyltransferase (GNMT). GNMT is a S-adenosylmethionine (SAM)-dependent methyltransferase which catalyses the transfer of the methyl group on SAM to the amino acid glycine to generate N-methyl glycine (sarcosine), a compound with poorly defined biological functions. Previous studies have suggested that GNMT may act as a tumour-susceptibility gene in prostate cancer, although the mechanisms by which GNMT acts in prostate cancer remain obscure. To ascertain the role of GNMT in prostate cancer, I have investigated GNMT expression and its regulation by AR. I show that GNMT expression is stimulated by androgen in AR-expressing cells and that the stimulation occurs at the mRNA and protein levels. I have identified an androgen-response element (ARE) within the first exon of the GNMT gene and demonstrated that AR binds to this element in vitro and in vivo. To investigate the role of GNMT in the androgen-mediated development of prostate cancer, I performed microarray analysis of LNCaP cells treated with two different GNMT small interference RNAs (siRNAs). I identified a cohort of genes that are differentially expressed upon GNMT knockdown, several of which have been implicated in cell cycle progression and motility. Finally, I have shown that GNMT over-expression impaired LNCaP cell migration in vitro, but did not affect LNCaP cell growth. Together, these studies identify GNMT as a direct transcriptional target of the AR and provide evidence for a role for GNMT in the androgen-mediated development and progression of prostate cancer.