Objective: To study the effect of traditional chinese medicine (TCM) compound on myeloid leukemia cells and to explore its anti-leukemic mechanism.
Methods: Myeloid leukemia cell lines were cultured in vitro and treated with TCM compound. The proliferation of the leukemia cells was measured by CCK8 method. The differentiation of the leukemia cells was evaluated by using Wright＇s staining method and by light microscopy, and the expression of differentiation-related surface antigens such as CD11B was measured and by flow cytometry, the apoptosis of the leukemia cells was detected by flow cytometry with using Annexin V staining.
Results: Compared with untreated 4 leukemia cell lines HL-60, MOLM-13, MV4-11, AML-M5, the proliferations of 4 leukemia cells treated with different concentrations of TCM compound decreased (P<0.05), and their proliferation inhibition were in a dose-dependent manner (r=0.9236; r=0.7488; r=0.8889; r=0.8119); compared with HL-60 and AML-M5 leukemia cells, the drug-treated 2 leukemia cells displayed obvious differentiated changes; compared with untreated HL-60 leukemia cell line, the expression of surface antigen CD11B increased by 85%±7.13% in HL-60 cells treated IC50 concentration of drug; compared with untreated AML-M5 leukemia cell line, the apoptotic rate of AML-M5 treated with 1.5 and 2 μl doses of TCM compound increased. (P<0.05).
Conclusion: The traditional chinese medicine compound may inhibit the proliferation of leukemia cell lines mainly by inducing leukemia cell differentiation and apoptosis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2019.02.015 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Long non-coding RNAs (lncRNAs) and RNA N⁶-methyladenosine (m A) have been linked to leukemia drug resistance. However, whether and how lncRNAs and m A coordinately regulate resistance remain elusive. Here, we show that many differentially expressed lncRNAs enrich m A, and more lncRNAs tend to have higher m A content in CML cells resistant to tyrosine kinase inhibitors (TKIs).
View Article and Find Full Text PDFThe significance of endogenous immune surveillance in acute lymphoblastic leukemia (ALL) remains controversial. Using clinical B-ALL samples and a novel mouse model, we show that neoantigen-specific CD4+ T cells are induced to adopt type-1 regulatory (Tr1) function in the leukemia microenvironment. Tr1s then inhibit cytotoxic CD8+ T cells, preventing effective leukemia clearance.
View Article and Find Full Text PDFAcute myeloid leukemia (AML) that is relapsed and/or refractory post-allogeneic hematopoietic cell transplantation (HCT) is usually fatal. In a prior study, we demonstrated that AML relapse in high-risk patients was prevented by post-HCT immunotherapy with Epstein-Barr virus (EBV)-specific donor CD8 T cells engineered to express a high-affinity Wilms Tumor Antigen 1 (WT1)-specific T-cell receptor (TTCR- C4). However, in the present study, infusion of EBV- or Cytomegalovirus (CMV)-specific T did not clearly improve outcomes in fifteen patients with active disease post-HCT.
View Article and Find Full Text PDFAdvances and Challenges in Quizartinib-Based FLT3 Inhibition for Acute Myeloid Leukemia: Mechanisms of Resistance and Prospective Combination Therapies.
Eur J Haematol
January 2025
Hematology Unit, Azienda Ospedaliera Annunziata, Cosenza, Italy.
FLT3 mutations are among the most common genetic alterations in acute myeloid leukemia (AML) and are associated with poor prognosis. Significant advancements have been made in developing FLT3 inhibitors (FLT3Is), such as quizartinib, which have improved treatment outcomes in both newly diagnosed and relapsed/refractory AML. Resistance to FLT3Is remains a major clinical challenge, driven by diverse mechanisms including FLT3 point mutations, cellular escape pathways, and the influence of the bone marrow microenvironment.
View Article and Find Full Text PDFExosomal circ_0006896 promotes AML progression via interaction with HDAC1 and restriction of antitumor immunity.
Mol Cancer
January 2025
Department of Hematology, Qilu Hospital of Shandong University, No.117, West of Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Background: Drug resistance and immune escape continue to contribute to poor prognosis in AML. Increasing evidence suggests that exosomes play a crucial role in AML immune microenvironment.
Methods: Sanger sequencing, RNase R and fluorescence in situ hybridization were performed to confirm the existence of circ_0006896.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!