Among the different types of cancer affecting the central nervous system (CNS), glioblastoma (GB) is classified by the World Health Organization (WHO) as the most common and aggressive CNS cancer in adults. GB incidence is more frequent among persons aged 45-55 years old. GB treatments are based on tumor resection, radiation, and chemotherapies. The current development of novel molecular biomarkers (MB) has led to a more accurate prediction of GB progression. Moreover, clinical, epidemiological, and experimental studies have established genetic variants consistently associated with the risk of suffering GB. However, despite the advances in these fields, the survival expectancy of GB patients is still shorter than 2 years. Thus, fundamental processes inducing tumor onset and progression remain to be elucidated. In recent years, mRNA translation has been in the spotlight, as its dysregulation is emerging as a key cause of GB. In particular, the initiation phase of translation is most involved in this process. Among the crucial events, the machinery performing this phase undergoes a reconfiguration under the hypoxic conditions in the tumor microenvironment. In addition, ribosomal proteins (RPs) have been reported to play translation-independent roles in GB development. This review focuses on the research elucidating the tight relationship between translation initiation, the translation machinery, and GB. We also summarize the state-of-the-art drugs targeting the translation machinery to improve patients' survival. Overall, the recent advances in this field are shedding new light on the dark side of translation in GB.
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http://dx.doi.org/10.3389/fcell.2023.1086964 | DOI Listing |
mBio
January 2025
Analytical Biochemistry and Proteomics Unit, Instituto de Investigaciones Biológicas Clemente Estable and Institut Pasteur de Montevideo, Montevideo, Uruguay.
Unlabelled: Mycobacteria, including pathogens like , exhibit unique growth patterns and cell envelope structures that challenge our understanding of bacterial physiology. This study sheds light on FhaA, a conserved protein in , revealing its pivotal role in coordinating cell envelope biogenesis and asymmetric growth. The elucidation of the FhaA interactome in living mycobacterial cells reveals its participation in the protein network orchestrating cell envelope biogenesis and cell elongation/division.
View Article and Find Full Text PDFiScience
January 2025
Department of Experimental Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Cdc25C undergoes a sudden and substantial gel mobility shift at M-phase onset, correlating with abrupt activation of both Cdc25C and Cdk1 activities. A positive feedback loop between Cdk1 and Cdc25C has been used to explain this hallmark phenomenon. Here, we demonstrate that the M-phase supershift and robust activation of Cdc25C are due to the site-comprehensive phosphorylation of its long intrinsically disordered regulatory domain without requiring Cdk1 or other major mitotic kinase activities.
View Article and Find Full Text PDFMol Plant
January 2025
Division of Applied Life Sciences (BK21(+)), Plant Biological Rhythm Research Center and PMBBRC, Gyeongsang National University, Jinju-52828, Korea. Electronic address:
The intricate interplay between cellular circadian rhythms, primarily manifested in the chloroplast redox oscillations-characterized by diel hyperoxidation/reduction cycles of 2-Cys Peroxiredoxins-and the nuclear transcription/translation feedback loop (TTFL) machinery within plant cells, demonstrates a remarkable temporal coherence. However, the molecular mechanisms underlying the integration of these circadian rhythms remain elusive. Here, we elucidate that the chloroplast redox protein, NADPH-dependent thioredoxin reductase type-C (NTRC), modulates the integration of the chloroplast redox rhythms and nuclear circadian clocks by regulating intracellular levels of reactive oxygen species and sucrose.
View Article and Find Full Text PDFPost-translational modifications play crucial roles in viral infections, yet many potential modifications remain unexplored in orthoflavivirus biology. Here we demonstrate that the UFMylation system, a post-translational modification system that catalyzes the transfer of UFM1 onto proteins, promotes infection by multiple orthoflaviviruses including dengue virus, Zika virus, West Nile virus, and yellow fever virus. We found that depletion of the UFMylation E3 ligase complex proteins UFL1 and UFBP1, as well as other UFMylation machinery components (UBA5, UFC1, and UFM1), significantly reduces infectious virion production for orthoflaviviruses but not the hepacivirus, hepatitis C.
View Article and Find Full Text PDFFEBS Lett
January 2025
Roche Pharma Research and Early Development (pRED), Large Molecule Research, Roche Innovation Center Munich, Penzberg, Germany.
The diphthamide modification of eukaryotic translation elongation factor (eEF2) is important for accurate protein synthesis. While the enzymes for diphthamide synthesis are known, coordination of eEF2 synthesis with the diphthamide modification to maintain only modified eEF2 is unknown. Physical and genetic interactions extracted from BioGRID show a connection between diphthamide synthesis enzymes and chaperones in yeast.
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