Objective: To investigate the effect of norcantharidin (NCTD) to proliferation of leukemia cells through disrupting key regulators of sonic Hedgehog (SHH) pathway and its downstream transcription factor SOX2.
Methods: CCK8 was used to detected the HL60 and NB4 cells after inhibited by NCTD, SMO and GLI1 inhibitor for 24 hours. Expression level of SMO, GLI1 and SOX2 in HL60 cells with NCTD treatment was detected by immunoblot. HL60 cells were transfected with pcDNA3.1 plasmid expressing GLI1 or SOX2. Empty vector and pcDNA3. 1-EGFP were divided into negative and positive control group, respectively. The expression of exogenous GLI1 or SOX2 in HL60 cells was confirmed by immunoblot, and growth curve of HL60 cell was checked by CCK8. Proliferation of genetic modified HL60 cells treated by various dose of NCTD was detected.
Results: NCTD, SMO/GLI1 inhibitors could inhibit the proliferation of NB4 and HL60 cells in a dose-dependent manner. Compared with solvent (DMSO)-treated control group, NCTD remarkably decreased protein level of SMO, GLI1 and SOX2. GLI1 and SOX2 were overexpressed in HL60 cells as compared with pcDNA3.1 empty vector-transfected group. Growth curve demonstrated significant proliferative advantage of GLI1/SOX2-transfected cells. CCK8 assay indicated that GLI1/SOX2-overexpressed HL60 cells were more resistant to NCTD treatment.
Conclusion: NCTD attenuates HL60 proliferation via targeting the Hedgehog/SOX2 axis.
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http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2021.01.005 | DOI Listing |
Part Fibre Toxicol
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IUF - Leibniz Research Institute for Environmental Medicine, Auf'm Hennekamp 50, 40225, Düsseldorf, Germany.
Background: Inhalation of combustion-derived nanoparticles may contribute to the development or exacerbation of inflammatory lung diseases by direct interaction with neutrophilic granulocytes. Earlier studies have shown that exposure of human neutrophils to carbon nanoparticles ex vivo causes a prolongation of cellular life by the reduction of apoptosis rates. Accordingly, reduced neutrophil apoptosis rates were observed in neutrophils from bronchoalveolar lavages from carbon nanoparticle-exposed animals.
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March 2025
Department of Hematology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong, China.
Introduction: Natural killer (NK) cells, which exert spontaneous cytotoxicity against infectious diseases and cancer, also play an important role in leukemia therapy. Despite the success of NK-based therapy in the treatment of myeloid leukemia, the potential use of NK alloreactivity in these hematologic malignancies remains elusive. The aim of the present study was to investigate whether allogeneic NK cells combined with aclacinomycin (ACM) could enhance anti-leukemic functionality against an acute myeloid leukemia (AML) cell line and to clarify the underlying mechanism.
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March 2025
State Key Laboratory of Phytochemistry and Natural Medicines in West China, and Yunnan Characteristic Plant Extraction Laboratory, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China.
Six undescribed lindenane sesquiterpenoid dimers (LSDs), shimianolides A-F (-), were isolated from the whole plants of var. . Shimianolides A-C (-) represent an unprecedented class of LSDs, distinguished by a highly fused 3/5/6/6/6/5/6/6/5/3 decacyclic scaffold.
View Article and Find Full Text PDFNat Prod Res
March 2025
Laboratory of Medicinal Chemistry, Chulabhorn Research Institute, Bangkok, Thailand.
The chemical investigation of the crude dichloromethane from the stems led to the isolation of two new prenylated pyranoflavanones, dereticulatinal () and dereticulatinone (). The structures were established by spectroscopic analysis and chemical transformation, and the absolute configurations of these isolates were deduced through CD comparison with that of lupinifolin. The cancer cytotoxicity study revealed that compound showed cytotoxicity against MOLT-3 cell with an IC value of 40.
View Article and Find Full Text PDFAnticancer Res
March 2025
Department of Laboratory Medicine, Institute of Science Tokyo, Tokyo, Japan
Background/aim: The Hippo signaling pathway is involved in cell proliferation through the regulation of its downstream molecule YAP. The dysregulation of Hippo signaling is associated with cancer cell proliferation. This study aimed to investigate the effects of YAP inhibitors and activators on the proliferation of human leukemia cell lines to examine whether YAP functions as a tumor suppressor or promoter.
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