Microbial fuel cell (MFC) is a promising technology that utilizes exoelectrogens cultivated in the form of biofilm to generate power from various types of sources supplied. A metal-reducing pathway is utilized by these organisms to transfer electrons obtained from the metabolism of substrate from anaerobic respiration extracellularly. A widely established model organism that is capable of extracellular electron transfer (EET) is Shewanella oneidensis. This review highlights the strategies used in the transformation of S. oneidensis and the recent development of MFC in terms of intervention through genetic modifications. S. oneidensis was genetically engineered for several aims including the study on the underlying mechanisms of EET, and the enhancement of power generation and wastewater treating potential when used in an MFC. Through engineering S. oneidensis, genes responsible for EET are identified and strategies on enhancing the EET efficiency are studied. Overexpressing genes related to EET to enhance biofilm formation, mediator biosynthesis, and respiration appears as one of the common approaches.
Glioblastoma (GBM) mesenchymal (MES) transition can be regulated by long non-coding RNAs (lncRNAs) via modulation of various factors (Epithelial-to-Mesenchymal (EMT) markers, biological signalling, and the extracellular matrix (ECM)). However, understanding of these mechanisms in terms of lncRNAs is largely sparse. This review systematically analysed the mechanisms by which lncRNAs influence MES transition in GBM from a systematic search of the literature (using PRISMA) performed in five databases (PubMed, MEDLINE, EMBASE, Scopus, and Web of Science). We identified a total of 62 lncRNAs affiliated with GBM MES transition, of which 52 were upregulated and 10 were downregulated in GBM cells, where 55 lncRNAs were identified to regulate classical EMT markers in GBM (E-cadherin, N-cadherin, and vimentin) and 25 lncRNAs were reported to regulate EMT transcription factors (ZEB1, Snai1, Slug, Twist, and Notch); a total of 16 lncRNAs were found to regulate the associated signalling pathways (Wnt/β-catenin, PI3k/Akt/mTOR, TGFβ, and NF-κB) and 14 lncRNAs were reported to regulate ECM components (MMP2/9, fibronectin, CD44, and integrin-β1). A total of 25 lncRNAs were found dysregulated in clinical samples (TCGA vs. GTEx), of which 17 were upregulated and 8 were downregulated. Gene set enrichment analysis predicted the functions of HOXAS3, H19, HOTTIP, MEG3, DGCR5, and XIST at the transcriptional and translational levels based on their interacting target proteins. Our analysis observed that the MES transition is regulated by complex interplays between the signalling pathways and EMT factors. Nevertheless, further empirical studies are required to elucidate the complexity in this process between these EMT factors and the signalling involved in the GBM MES transition.