Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukemia remains a fatal disease for most patients and effective therapeutic strategies are urgently required. Typhaneoside (TYP) is a major flavonoid in the extract of Pollen Typhae, showing significant biological and pharmacological effects. In the present study, we explored the effects of TYP on acute myeloid leukemia (AML) progression. The results indicated that TYP markedly reduced the cell viability of AML cells and arrested the cell cycle at the G2/M phase by regulating the expression of associated proteins. In addition, TYP significantly induced apoptosis in AML cells by promoting the activation of Caspase-3. Intracellular and mitochondrial reactive oxygen species (ROS) accumulation were highly detected in AML cells after treatment with TYP. Moreover, TYP clearly induced ferroptosis in AML cells, and this process was iron-dependent and attendant with mitochondrial dysfunction. We also found that TYP significantly triggered autophagy in AML cells by promoting the activation of AMP-activated protein kinase (AMPK) signaling, contributing to ferritin degradation, ROS accumulation and ferroptotic cell death ultimately. In conclusion, the findings above provided solid evidences that TYP could be a promising therapeutic agent to prevent AML progression by inducing apoptosis, ROS production, autophagy and ferroptosis.
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PMID:Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy. 3130 67

Circular RNAs (circRNAs) are relevant to progression of acute myeloid leukemia (AML). Nevertheless, how and whether hsa_circ_0002483 (circ_0002483) participates in AML progression are largely uncertain. The bone marrow samples were harvested from 31 AML patients or 31 normal subjects. circ_0002483, microRNA (miR)-758-3p and myelocytomatosis oncogene (MYC) abundances were examined via quantitative reverse transcription polymerase chain reaction and western blot. Cell proliferation, cycle process and apoptosis were analyzed via Cell Counting Kit-8 (CCK-8), flow cytometry, caspase 3 activity and related protein levels. Target relationship was investigated by dual-luciferase reporter assay and RNA immunoprecipitation. Circ_0002483 expression was elevated in AML patients and cells. circ_0002483 silence constrained AML cell proliferation and facilitated cell cycle arrest and apoptosis. miR-758-3p was reduced in AML and decreased via circ_0002483. miR-758-3p down-regulation mitigated the inhibitive influence of circ_0002483 interference on AML progression. MYC was decreased by miR-758-3p, and circ_0002483 could regulate MYC expression by miR-758-3p. miR-758-3p overexpression restrained cell proliferation, and promoted cycle arrest and apoptosis via decreasing MYC. Circ_0002483 knockdown repressed AML cell proliferation and promoted cycle arrest and apoptosis via controlling miR-758-3p/MYC axis. This article is protected by copyright. All rights reserved.
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PMID:Hsa_circ_0002483 regulates miR-758-3p/MYC axis to promote acute myeloid leukemia progression. 3328 85