Epithelial-mesenchymal transition (EMT) induced by microenvironment stimuli can be attributed to the transcriptional regulation of epithelial and mesenchymal phenotypes. Here we show how EMT is coordinated with cancer metabolism, an emerging hallmark of tumorigenesis.
Targeting metabolic flexibility via angiopoietin-like 4 protein sensitizes metastatic cancer cells to chemotherapy drugs.
Cell line
View SamplesPseudomonas aeruginosa is a leading causative agent in nosocomial infections, which is attributed to its ability to form robust biofilms and engage a series of virulence mechanisms. Cyclic-di-GMP (c-di-GMP), a secondary messenger found in most bacterial species, is well known to regulate P. aeruginosa biofilm formation. High intracellular c-di-GMP content enhances biofilm formation, while a reduction of the c-di-GMP content in biofilm cells leads to biofilm dispersal. It remains unclear how biofilm dispersal through c-di-GMP reduction will ‘prepare’ the dispersed cells for their subsequent planktonic lifestyle. Here, we show that cells with high and low intracellular c-di-GMP contents have distinct transcriptome profiles. Interestingly, quorum-sensing (QS)-controlled virulence factors such as rhamnolipids and pyocyanin were found to be highly expressed in cells with low intracellular c-di-GMP content compared to cells with higher c-di-GMP content. This correlates well with their intracellular survival rates and cytotoxicity after in vitro exposure to murine macrophages. Our data suggests that biofilm dispersal through c-di-GMP manipulation might induce QS-regulated virulence during infections.
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Disease, Cell line
View Samples