Study of Expression of MST3 in Myeloid Leukaemia

Medical Sciences, Journal Year: 2025, Volume and Issue: 13(2), P. 33 - 33

Published: April 1, 2025

Myeloid leukaemia (ML) is a cancer that occurs by the accumulation of abnormally multiplied myeloid cells in bone marrow, peripheral blood, and other related tissue. MST3 gene GCK family has role apoptosis, along with cellular functions like differentiation, cell cycle, metabolism, others. Objectives: The objectives this study were to count RBCs WBCs, expression ML control samples, perform an silico correlation on KRAS NRAS genes. Methods: counting WBCs was carried out using hemacytometer, studied RT-PCR, GEPIA. Results: RBC WBC levels differed from levels, found be upregulated comparison controls, 2.90–8.65-fold change, significant p-value > 0.05. A positive also between genes, r value correlation. Conclusions: From study, it could deduced might have pathogenesis, but further research needed its progression disease.

Language: Английский

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Inhibition of the CXCR4/PLC Signaling Increases Dexamethasone-Induced Sensitivity by Activating the Mitochondrial Apoptotic Pathway in B-Cell Acute Lymphoblastic Leukemia

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3489 - 3489

Published: April 8, 2025

Understanding the mechanisms underlying glucocorticoid (GC) resistance in B-cell acute lymphoblastic leukemia (B-ALL) is essential to improve survival rates relapsed children. We previously showed that GCs paradoxically induced their own B-ALL through CXCR4/PLC signaling, and inhibition of this pathway significantly reverses GC cells improves GC-treated NSG mice vivo. Here, we sought determine whether enhancement sensitivity via axis associated with disruption mitochondrial pathway. Analysis our previous transcriptomic data revealed B-ALL, PLC inhibitor U73122 compromised multiple metabolic pathways related reprogramming, function, oxidative stress. Inhibition U73122, protein kinase C GF109203X, or CXCR4 AMD3100 potentiated dexamethasone (Dex)-induced membrane potential depolarization, reactive oxygen species production, cytochrome c release, caspase-3 activation, decreased O2 consumption cells. These observations were also confirmed after Dex treatment a Nalm-6 cell line transfected small interfering RNA. Moreover, co-treatment CXCR4, PKC, inhibitors increased levels pro-apoptotic BIM (BCL-2 interacting mediator death) and, consequently, promoted death process. Together, these findings suggest reduces efficacy by limiting apoptotic activity.

Language: Английский

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CD40 promotes AML survival via non-canonical NF-κB signaling and aberrant lipid metabolism

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 156, P. 114665 - 114665

Published: April 18, 2025

Language: Английский

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A Novel Single-Color FRET Sensor for Rho-Kinase Reveals Calcium-Dependent Activation of RhoA and ROCK

Sensors, Journal Year: 2024, Volume and Issue: 24(21), P. 6869 - 6869

Published: Oct. 26, 2024

Ras homolog family member A (RhoA) acts as a signaling hub in many cellular processes, including cytoskeletal dynamics, division, migration, and adhesion. RhoA activity is tightly spatiotemporally controlled, but whether downstream effectors share these activation dynamics unknown. We developed novel single-color FRET biosensor to measure Rho-associated kinase (ROCK) with high spatiotemporal resolution live cells. report the validation of Rho-Kinase Activity Reporter (RhoKAR) biosensor. RhoKAR was specific ROCK insensitive PKA activity. then assessed mechanisms mouse fibroblasts. Increasing intracellular calcium ionomycin increased depleting EGTA decreased also investigated intermediates this process. Blocking calmodulin or CaMKII prevented calcium-dependent ROCK. These results indicate that by fibroblasts occurs CaM/CaMKII.

Language: Английский

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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

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