RESUMEN
The synchronous bioelectricity generation and dissimilatory nitrate reduction to ammonium (DNRA) pathway in Klebsiella variicola C1 was investigated. The presence of bioelectricity facilitated cell growth on the anodic biofilms, consequently enhancing the nitrate removal efficiency decreasing total nitrogen levels and causing a negligible accumulation of NO2- in the supernatant. Genomic analysis revealed that K. variicola C1 possessed a complete DNRA pathway and largely annotated electron shuttles. The up-regulated expression of genes narG and nirB, encoding nitrite oxidoreductase and nitrite reductase respectively, was closely associated with increased extracellular electron transfer (EET). High-throughput sequencing analysis was employed to investigate the impact of bioelectricity on microbial community composition within cathodic biofilms. Results indicated that Halomonas, Marinobacter and Prolixibacteraceae were enriched at the cathode electrodes. In conclusion, the integration of a DNRA strain with MFC facilitated the efficient removal of wastewater containing high concentrations of NO3- and enabled the environmentally friendly recovery of NH4+.
Asunto(s)
Compuestos de Amonio , Fuentes de Energía Bioeléctrica , Biopelículas , Electrodos , Nitratos , Fuentes de Energía Bioeléctrica/microbiología , Nitratos/metabolismo , Compuestos de Amonio/metabolismo , Klebsiella/metabolismo , Klebsiella/genética , Aguas Residuales/microbiología , Microbiota/fisiología , Oxidación-Reducción , ElectricidadRESUMEN
Cisplatin-based chemotherapy is the standard treatment for metastatic ovarian cancer (OC). However, chemoresistance continues to pose significant clinical challenges. Recent research has highlighted the baculoviral inhibitor of the apoptosis protein repeat-containing 5 (BIRC5) as a member of the inhibitor of the apoptosis protein (IAP) family. Notably, BIRC5, which has robust anti-apoptotic capabilities, is overexpressed in numerous cancers. Its dysfunction has been linked to challenges in cancer treatment. Yet, the role of BIRC5 in the chemoresistance of OC remains elusive. In our present study, we observed an upregulation of BIRC5 in cisplatin-resistant cell lines. This upregulation was associated with enhanced chemoresistance, which was diminished when the expression of BIRC5 was silenced. Intriguingly, BIRC5 exhibited a high number of N6-methyladenosine (m6A) binding sites. The modification of m6A was found to enhance the expression of BIRC5 by recognizing and binding to the 3'-UTR of mRNA. Additionally, the insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) was shown to stabilize BIRC5 mRNA, synergizing with METTL3 and intensifying chemoresistance. Supporting these in vitro findings, our in vivo experiments revealed that tumors were significantly smaller in size and volume when BIRC5 was silenced. This reduction was notably counteracted by co-silencing BIRC5 and overexpressing IGF2BP1. Our results underscored the pivotal role of BIRC5 in chemoresistance. The regulation of its expression and the stability of its mRNA were influenced by m6A modifications involving both METTL3 and IGF2BP1. These insights presented BIRC5 as a promising potential therapeutic target for addressing cisplatin resistance in OC.