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International audienceNitrogen (N) is a major fertiliser for agriculture and food production. About 67.84 million tons of N are annually applied to agricultural fields, without which nearly half of the world’s population would not be alive today. Returning plant residues to the soil is an alternative and sustainable way of N fertilisation. Although impacts of returning plant residues on plant available N in soil have been widely studied, there is still no systematic review of their mechanisms and models. In this review we highlight the following advances: (1) When plant residues are returned to the soil, N undergoes biotic immobilisation–remineralisation, abiotic immobilisation, soil organic N mineralisation and plant residue organic N mineralisation. (2) Plant residues modify inorganic N fate using three mechanism mineralisation, immobilisation–mineralisation and immobilisation, depending on plant residue nature and soil properties. (3) The use of plant residue C/N ratio is not always effective to predict the effect of plant residues. Instead, soil properties and the forms of carbon and nitrogen should be considered. (4) Mineralisation always promotes N uptake by crops and increases the risk of N loss. In addition, although net immobilisation is involved in immobilisation–mineralisation and immobilisation, it does not necessarily induce lower crop nitrogen uptake. Results also depend on the synchronism between the changing soil inorganic N and the crop N uptake. (5) N loss during mineralisation can be reduced by an immobiliser. Net N immobilisation during immobilisation–mineralisation and immobilisation can be reduced by changing the timing of ploughing and fertilising or by changing the plant residues placement

Neoplastic cells use various intercellular communication mechanisms in order to adapt to the local microenvironment, manipulate the immune system, and facilitate metastasis. Exosomes release is a new mechanism of cell-to-cell communication. These nanovesicles enclose various types of molecules including lipids, proteins, DNA, messenger RNA (mRNA) and non-coding RNAs [microRNA and long non-coding RNA (lncRNA)]. lncRNAs are over 200 nt long transcripts, that exhibit no coding potential, but are crucial regulators of physiological processes and are deregulated in cancer. In this review, we will discuss the role of exosomal lncRNAs in cancer, which is an incipient research field that could bring new insights to the vast domain of intercellular communication. Exosomal lncRNAs seem to be promising biomarkers for any type of cancer. The exact role of exosomal lncRNAs is not fully revealed. Several studies show that cancer derived exosomal lncRNAs are functional and can transmit to neighboring cells different phenotypic patterns, like drug resistance and increased angiogenesis. We further discuss the mechanistic function of exosomal lncRNAs, and hypothesize that the crowded exosomal content can be a suitable place of RNA species crosstalk. Finally, we assume that lncRNAs could be a loading vehicle for miRNAs, mRNAs and other complex molecules into the exosome but future studies are required to confirm these hypotheses.

The cancer-risk-associated rs6983267 single nucleotide polymorphism (SNP) and the accompanying long noncoding RNA in the highly amplified 8q24.21 region have been implicated in cancer predisposition, although causality has not been established. Here, using allele-specific transgenic mice, we demonstrate that overexpression leads to spontaneous myeloid malignancies. We further identified that is overexpressed in bone marrow and peripheral blood of myelodysplastic/myeloproliferative neoplasms (MDS/MPN) patients. induces global deregulation of gene expression by down-regulating EZH2 in vitro and in vivo in an allele-specific manner. We also identified a novel non-APOBEC, non-ADAR, RNA editing at the SNP locus in MDS/MPN patients and-transgenic mice. The RNA transcribed from the SNP locus in malignant hematopoietic cells have different allelic composition from the corresponding genomic DNA, a phenomenon rarely observed in normal cells. Our findings provide fundamental insights into the functional role of rs6983267 SNP and in myeloid malignancies.

We thank the MDACC Cytogenetics and Cell Authentication Core for technical assistance in the cytogenetic analysis.

It is now well known that non-coding RNAs (ncRNAs), rather than protein-coding transcripts, are the preponderant RNA transcripts. NcRNAs, particularly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are widely appreciated as pervasive regulators of multiple cancer hallmarks such as proliferation, apoptosis, invasion, metastasis, and genomic instability. Despite recent discoveries in cancer therapy, resistance to chemotherapy, radiotherapy, targeted therapy, and immunotherapy continue to be a major setback. Recent studies have shown that ncRNAs also play a major role in resistance to different cancer therapies by rewiring essential signaling pathways. In this review, we present the intricate mechanisms through which dysregulated ncRNAs control resistance to the four major types of cancer therapies. We will focus on the current clinical implications of ncRNAs as biomarkers to predict treatment response (intrinsic resistance) and to detect resistance to therapy after the start of treatment (acquired resistance). Furthermore, we will present the potential of targeting ncRNA to overcome cancer treatment resistance, and we will discuss the challenges of ncRNA-targeted therapy—especially the development of delivery systems.

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In this study with large number of patients, PDCD1 and CTLA-4 expression is significantly higher in squamous carcinoma and current/former smokers. Higher expression of CTLA-4, but not PDCD1 predicts worse survival.