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The syncytium is a unique plant root organ whose differentiation is induced by plant-parasitic cyst nematodes to create a source of nourishment. Syncytium formation involves the redifferentiation and fusion of hundreds of root cells. The underlying regulatory networks that control this unique change of plant cell fate are not understood. Here, we report that a strong down-regulation of Arabidopsis (Arabidopsis thaliana) microRNA396 (miR396) in cells giving rise to the syncytium coincides with the initiation of the syncytial induction/formation phase and that specific miR396 up-regulation in the developed syncytium marks the beginning of the maintenance phase, when no new cells are incorporated into the syncytium. In addition, our results show that miR396 in fact has a role in the transition from one phase to the other. Expression modulations of miR396 and its Growth-Regulating Factor (GRF) target genes resulted in reduced syncytium size and arrested nematode development. Furthermore, genome-wide expression profiling revealed that the miR396-GRF regulatory system can alter the expression of 44% of the more than 7,000 genes reported to change expression in the Arabidopsis syncytium. Thus, miR396 represents a key regulator for the reprogramming of root cells. As such, this regulatory unit represents a powerful molecular target for the parasitic animal to modulate plant cells and force them into novel developmental pathways.
The Arabidopsis MicroRNA396-GRF1/GRF3 Regulatory Module Acts as a Developmental Regulator in the Reprogramming of Root Cells during Cyst Nematode Infection1,[W][OA]
Tarek Hewezi, Tom R. Maier, Dan Nettleton, and Thomas J. Baum*
Long non-coding RNAs (lncRNAs) have been implicated in pathogenesis of various cancers, including lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD). We used cBioPortal to analyze lncRNA alteration frequencies and their ability to predict overall survival (OS) using 504 LUSC and 522 LUAD samples from The Cancer Genome Atlas (TCGA) database. In LUSC, 624 lncRNAs had alteration rates > 1% and 64 > 10%. In LUAD 625 lncRNAs had alteration rates > 1% and 36 > 10%. Among those, 620 lncRNAs had alteration frequencies > 1% in both LUSC and LUAD, while 22 were LUSC-specific and 23 were LUAD-specific. Twenty lncRNAs had alteration frequencies > 10% in both LUSC and LUAD, while 44 were LUSC-specific and 16 were LUAD specific. Genome ontology and pathway analyses produced similar results for LUSC and LUAD. Two lncRNAs (IGF2BP2-AS1 and DGCR5) correlated with better OS in LUSC, and three (MIR31HG, CDKN2A-AS1 and LINC01600) predicted poor OS in LUAD. Chip-seq and luciferase reporter assays identified potential IGF2BP2-AS1, DGCR5 and LINC01600 promoters and enhancers. This study presented lncRNA landscapes and revealed differentially expressed, highly altered lncRNAs in LUSC and LUAD. LncRNAs that act as oncogenes and lncRNA-regulating transcription factors provide novel targets for anti-lung cancer therapeutics.
lung squamous cell carcinoma, lung adenocarcinoma, long non-coding RNA, overall survival, gene regulation
LncRNAs are altered in lung squamous cell carcinoma and lung adenocarcinoma
Bing Liu,#1 Yifei Chen,#1 and Jiong Yang1
2017 Apr 11
Heart disease and cancer are the first and second leading causes of death in the United States. Age-standardized death rates (risk) have declined since the 1960s for heart disease and for cancer since the 1990s, whereas the overall number of heart disease deaths declined and cancer deaths increased. We analyzed mortality data to evaluate and project the effect of risk reduction, population growth, and aging on the number of heart disease and cancer deaths to the year 2020.
We used mortality data, population estimates, and population projections to estimate and predict heart disease and cancer deaths from 1969 through 2020 and to apportion changes in deaths resulting from population risk, growth, and aging.
We predicted that from 1969 through 2020, the number of heart disease deaths would decrease 21.3% among men (-73.9% risk, 17.9% growth, 34.7% aging) and 13.4% among women (-73.3% risk, 17.1% growth, 42.8% aging) while the number of cancer deaths would increase 91.1% among men (-33.5% risk, 45.6% growth, 79.0% aging) and 101.1% among women (-23.8% risk, 48.8% growth, 76.0% aging). We predicted that cancer would become the leading cause of death around 2016, although sex-specific crossover years varied.
Risk of death declined more steeply for heart disease than cancer, offset the increase in heart disease deaths, and partially offset the increase in cancer deaths resulting from demographic changes over the past 4 decades. If current trends continue, cancer will become the leading cause of death by 2020.
Heart Disease and Cancer Deaths — Trends and Projections in the United States, 1969-2020
Hannah K. Weir, PhD,corresponding author Robert N. Anderson, PhD, Sallyann M. Coleman King, MD, MSc, Ashwini Soman, MPH, Trevor D. Thompson, BS, Yuling Hong, MD, MS, PhD, Bjorn Moller, PhD, and Steven Leadbetter, MS