DNA methylation levels of TaP5CS and TaBADH are associated with enhanced tolerance to PEG-induced drought stress triggered by drought priming in wheat.

Drought priming is a promising strategy to enhance tolerance to recurred drought in wheat. However, the underlying mechanisms of priming-induced tolerance are far from clear. Here, three different priming intensities (P1D, P2D, P3D) and two varieties with different sensitivities to drought priming were used to investigate the effects and mechanisms of drought priming. Results showed light (P1D) or moderate (P2D) drought priming intensity induced positive effects for the drought sensitive variety (YM16), while high (P3D) priming intensity brought a negative impact on the plant drought resistant. For drought insensitive one (XM33), light priming intensity had no significant effect on tolerance to drought, while moderate or high intensity showed better priming effects. Moderate priming induced higher leaf water potential and also the osmolytes levels. Consistent with the proline and betaine, the related synthetic enzymatic activities, as well as the expression of TaP5CS and TaBADH were higher in P2D in YM16 and P3D in XM33. The contents of proline and betaine showed a positive correlation with activities of SOD, CAT, GR, AsA, and GSH contents, and a negative correlation with O2.-, H2O2, and MDA contents. Further analysis revealed CG demethylation of ATG-proximal regions in the promoter of TaP5CS and TaBADH were involved in promoting the synthesis of proline and betaine in primed plants. Collectively, these findings demonstrate drought priming effect was variety independent but depended on the priming severity, and demethylation of TaP5CS and TaBADH involved in the accumulation of osmolytes which contribute to the enhanced drought tolerance induced by priming.

Macrophages induce EMT to promote invasion of lung cancer cells through the IL-6-mediated COX-2/PGE2/ß-catenin signalling pathway.

Infiltration of macrophages plays a critical role in the connection between inflammation and cancer invasion; however, the molecular mechanism that enables this crosstalk remains unclear. This paper investigates a molecular link between infiltration of macrophages and metastasis of lung cancer cells. In this study, the macrophage density and cyclooxygenase-2 (COX-2) protein were examined in surgical specimens by immunohistochemistry (IHC), and the prostaglandin E2 (PGE2) levels were determined in the blood of 30 non-small cell lung cancer (NSCLC) patients using enzyme-linked immunosorbent assay (ELISA). We demonstrated that macrophage infiltration was significantly associated with elevated tumour COX-2 expression and serum PGE2 levels in NSCLC patients. Interestingly, the COX-2 and PGE2 levels as well as macrophages were poor predictors of NSCLC patient survival. THP-1-derived macrophages were co-cultured in vitro with A549 and H1299 lung cancer cells. In the co-culture process, interleukin-6 (IL-6) induced the COX-2/PGE2 pathway in lung cancer cells, which subsequently promoted ß-catenin translocation from the cytoplasm to the nucleus, resulting in epithelial-mesenchymal transition (EMT) and lung cancer cell invasion. Our findings show that the IL-6-dependent COX-2/PGE2 pathway induces EMT to promote invasion of tumour cells through ß-catenin activation during the interaction between macrophages and lung cancer cells, which suggests that inhibition of COX-2/PGE2 or macrophages has the potential to suppress metastasis of lung cancer cells.