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Myc hyperactivation coordinately regulates numerous metabolic processes to drive lymphomagenesis. Here, we elucidate the temporal and functional relationships between the medley of pathways, factors, and mechanisms that cooperate to control redox homeostasis in Myc-overexpressing B cell lymphomas. We find that Myc overexpression rapidly stimulates the oxidative pentose phosphate pathway (oxPPP), nucleotide synthesis, and mitochondrial respiration, which collectively steers cellular equilibrium to a more oxidative state.
View Article and Find Full Text PDFRe-Sensitization of Resistant Ovarian Cancer SKOV3/CDDP Cells to Cisplatin by Curcumin Pre-Treatment.
Int J Mol Sci
January 2025
Laboratory of Molecular Oncobiology, Institute of Gene Biology, Russian Academy of Sciences, 34/5 Vavilov Street, 119334 Moscow, Russia.
A major challenging problem facing effective ovarian cancer therapy is cisplatin resistance. Re-sensitization of cisplatin-resistant ovarian cancer cells to cisplatin (CDDP) has become a critical issue. Curcumin (CUR), the most abundant dietary polyphenolic curcuminoids derived from turmeric (), has achieved previously significant anti-cancer effects against human ovarian adenocarcinoma SKOV-3/CDDP cisplatin-resistant cells by inhibition the gene expression of the antioxidant enzymes (, , , and ), transcription factor and signaling pathway (//).
View Article and Find Full Text PDFDual Roles of Reducing Systems in Protein Persulfidation and Depersulfidation.
Antioxidants (Basel)
January 2025
Université de Lorraine, INRAE, IAM, F-54000 Nancy, France.
The oxidative modification of specific cysteine residues to persulfides is thought to be the main way by which hydrogen sulfide (HS) exerts its biological and signaling functions. Therefore, protein persulfidation represents an important thiol-switching mechanism as other reversible redox post-translational modifications. Considering their reductase activity but also their connections with proteins that generate HS and its related molecules, the glutaredoxin (GRX) and thioredoxin (TRX)-reducing systems have potential dual roles in both protein persulfidation and depersulfidation.
View Article and Find Full Text PDFSelenium Nucleophilicity and Electrophilicity in the Intra- and Intermolecular SN2 Reactions of Selenenyl Sulfide Probes.
Chemistry
January 2025
University of Padova: Universita degli Studi di Padova, Dipartimento di Scienze Chimiche, Via Marzolo 1, 35131, Padova, ITALY.
Chalcogenide exchange reactions are an important class of bimolecular nucleophilic substitution reactions (SN2) involving sulfur and selenium species as nucleophile, central atom, and/or leaving group, which are fundamental throughout redox biology and metabolism. While thiol-disulfide exchange reactions have been deeply investigated, those involving selenium are less understood, especially with regards to the polarised selenenyl sulfides RSe-SR' even though the directed reactivity of selenenyl sulfides is biologically crucial for selenoenzymes such as thioredoxin reductase (TrxR) and glutathione peroxidase (GPx). Synthetic methods to create asymmetric selenenyl sulfides with high regiochemical purity only emerged over the last five years; this functional group has already demonstrated powerful applications to cell biology, through probes for molecular imaging (e.
View Article and Find Full Text PDFResveratrol Reduces Cisplatin-induced Cochlear Hair Cell Pyroptosis by Inhibiting the mtROS/TXNIP/NLRP3 Pathway.
Comb Chem High Throughput Screen
January 2025
Department of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Background: Cisplatin is an effective anti-cancer drug with limited clinical applications due to ototoxicity. Resveratrol, known for its antioxidant and anti-inflammatory properties, has been reported to mitigate these adverse effects, although the underlying mechanism remains under-researched.
Objective: This study aimed to investigate the effects and underlying mechanisms of resveratrol on cisplatin-induced ototoxicity.
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