Anti-ECI2 monoclonal antibody, clone 2I5

Highly efficient somatic embryogenesis (SE) initiation systems are crucial for the clonal propagation and genetic transformation of Lilium Oriental x Trumpet hybrid. To elucidate the underlying mechanism of SE induction, we conducted de novo transcriptome sequencing of the roots at four different times in relation to SE initiation (0 days, control; 20 days, embryogenic callus induction (ECI) 1; 40 days, ECI2; 55 days, ECI3). A total of 4621, 7582, and 7427 differentially expressed genes (DEGs) were identified from the ECI1 vs. control, ECI2 vs. control, and ECI3 vs. control comparisons, respectively. The gene-enrichment analysis revealed 54 significant DEGs. Further analysis showed that the transcript levels of the auxin-related genes ARF9/15/16, the abscisic acid-related (ABA-related) genes PYL4/9, and stress-related transcription factors, including WRKY26, MYB36, NAC100, bHLH2/5/18/112, and HSP90, were increased at the ECI1 stage. ABI5 can influence the expression of stress-responsive genes as an ABA signalling regulator. The upregulated ABI5 could be caused by the increased ARF9/15/16, PYL4/9, WRKY26, MYB36, NAC100, bHLH2/5/18/112, and HSP90 at the ECI2 and ECI3 stages to regulate the ECI. These genes had the most abundant transcripts among the DEGs, indicating that auxin and stress-related signalling pathways are involved in SE initiation of Lilium spp.

Prostate cancer is the most common male cancer and androgen receptor (AR) is the major driver of the disease. Here we show that Enoyl-CoA delta isomerase 2 (ECI2) is a novel AR-target that promotes prostate cancer cell survival. Increased ECI2 expression predicts mortality in prostate cancer patients (p = 0.0086). ECI2 encodes for an enzyme involved in lipid metabolism, and we use multiple metabolite profiling platforms and RNA-seq to show that inhibition of ECI2 expression leads to decreased glucose utilization, accumulation of fatty acids and down-regulation of cell cycle related genes. In normal cells, decrease in fatty acid degradation is compensated by increased consumption of glucose, and here we demonstrate that prostate cancer cells are not able to respond to decreased fatty acid degradation. Instead, prostate cancer cells activate incomplete autophagy, which is followed by activation of the cell death response. Finally, we identified a clinically approved compound, perhexiline, which inhibits fatty acid degradation, and replicates the major findings for ECI2 knockdown. This work shows that prostate cancer cells require lipid degradation for survival and identifies a small molecule inhibitor with therapeutic potential.