Exploring miR-34a, miR-449, and ADAM2/ADAM7 Expressions as Potential Biomarkers in Male Infertility: A Combined In Silico and Experimental Approach

Biochemical Genetics, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 10, 2025

Language: Английский

Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation

Journal of the Egyptian National Cancer Institute, Journal Year: 2025, Volume and Issue: 37(1)

Published: March 10, 2025

Abstract Background To investigate the anticancer effects of 5-Fluorouracil (5-FU), thymoquinone (TQ), and/or coenzyme Q10 (CQ10), alone and combined, in HT29, SW480, SW620 human colorectal cancer (CRC) cell lines. Methods Cell cycle progression apoptosis were assessed by flow cytometry. Gene protein expression molecules involved (BLC2, survivin, BAX, Cytochrome-C, Caspase-3), (CCND1, CCND3, p21, p27), PI3K/AKT/mTOR/HIF1α oncogenic pathway, glycolysis (LDHA, PDH, PDHK1) also analysed quantitative RT-PCR Western blot. Oxidative stress markers (ROS/RNS, MDA, Protein carbonyl groups) antioxidants (GSH CAT) quantified ELISA. Results All treatments resulted depicted arrest apoptosis, with TQ demonstrating greater efficacy than CQ10, both without 5-FU. However, 5-FU/TQ/CQ10 triple therapy exhibited most potent pro-apoptotic activity all lines, portrayed lowest levels oncogenes BCL2, survivin) highest upregulation tumour suppressors (p21, p27, Caspase-3). The showed strongest suppression a concurrent increase its endogenous inhibitors (PTEN AMPKα) lines used. Additionally, favoured glucose oxidation upregulating while decreasing LDHA PDHK1 enzymes. displayed significant decline antioxidant increases oxidative markers. Conclusions This study is first to demonstrate superior compared 5-FU, CRC treatment. Moreover, this report reveal improved therapy, potentially through promoting phosphorylation, attenuating increasing stress-induced apoptosis. Graphical Human colon cells (HT29, & SW620) treated individually for 12h. related PI3K/AKT/mTOR glycolytic enzymes, measured. protocol revealed best

Language: Английский

Mitophagy in Doxorubicin-Induced Cardiotoxicity: Insights into Molecular Biology and Novel Therapeutic Strategies

Biomolecules, Journal Year: 2024, Volume and Issue: 14(12), P. 1614 - 1614

Published: Dec. 17, 2024

Doxorubicin is a chemotherapeutic drug utilized for solid tumors and hematologic malignancies, but its clinical application hampered by life-threatening cardiotoxicity, including cardiac dilation heart failure. Mitophagy, cargo-specific form of autophagy, specifically used to eliminate damaged mitochondria in autophagosomes through hydrolytic degradation following fusion with lysosomes. Recent advances have unveiled major role defective mitophagy the etiology DOX-induced cardiotoxicity. Moreover, specific interventions targeting this mechanism preserve mitochondrial function emerged as potential therapeutic strategies attenuate However, translation challenging because unclear mechanisms action pharmacological adverse effects. This review aims offer fresh perspectives on development cardiotoxicity investigate that focus improve management.

Language: Английский