AI Article Synopsis
- This study investigates the anticancer effects of betulinic acid (BA) on Jurkat cells, a type of leukemia cell line, focusing on its impact on cell growth and apoptosis.
- The research reveals that betulinic acid significantly reduces the proliferation of Jurkat cells, induces apoptosis in a dose- and time-dependent manner, and alters the cell cycle by increasing the proportion of cells in the G0/G1 phase while decreasing those in the S phase.
- Additionally, the treatment with betulinic acid leads to a notable decrease in the expression of cyclin D3 and bcl-xl, suggesting that its antitumor effects may stem from these molecular changes.
Article Abstract
Objective: To investigate the anticancer effects of betulinic acid (BA) on Jurkat cells in vitro and its molecular mechanism.
Methods: The effects of betulinic acid on the growth of Jurkat cells were studied by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5diphenyl-2H-tetrazolium (MTT) assay. Apoptosis was assessed by Hoechst33258 staining and annexin-V/PI double-labeled cytometry. The effect of betulinic acid on the cell cycle of Jurkat cells was studied by propidium iodide staining. RT-PCR and Western blot were used to analyze the changes of cyclin D3, bcl-xl mRNA and protein levels in Jurkat cells after treatment with betulinic acid.
Results: The proliferation of Jurkat cells was decreased in betulinic acid-treated group at a 24 h IC50 value of 70.0 micromol/L. The effect of betulinic acid to induce apoptosis in Jurkat cells was in a time- and dose-dependent manner. Jurkat cells treated with betulinic acid showed an increase of G0/G1 phase and decrease of S phase. The Jurkat cells treated with 0, 20, 60, 100 micromol/L betulinic acid for 24 h, showed an increased G0/G1 phase from 31.0% to 58.8%, whereas decreased S phase from 61.5% to 35.8%, respectively. PBMC was less sensitive to the cytotoxic effect of betulinic acid than Jurkat cells. The expression of cyclin D3, bcl-xl mRNA and protein were decreased sharply in Jurkat cells treated with betulinic acid.
Conclusion: Betulinic acid can inhibit the proliferation of Jurkat cells by regulating the cell cycle that arrests cells at G0/G1 phase and induces apoptosis in Jurkat cells. The antitumor effects of betulinic acid may be related to down-regulation of the expression of cyclin D3 and bcl-xl.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Potassium channels regulate membrane potential, calcium flux, cellular activation and effector functions of adaptive and innate immune cells. The voltage-activated Kv1.3 channel is an important regulator of T cell-mediated autoimmunity and microglia-mediated neuroinflammation.
View Article and Find Full Text PDFApigenin facilitates apoptosis of acute lymphoblastic leukemia cells via AMP-activated protein kinase-mediated ferroptosis.
Oncol Res
January 2025
Department of Microbiology, College of Preclinical Medicine, Zunyi Medical University, Zunyi, 563003, China.
Background: The outcomes of pediatric patients with acute lymphoblastic leukemia (ALL) remain far less than favorable. While apigenin is an anti-cancer agent, studies on the mechanism by which it regulates ALL cell cycle progression are inadequate. Ferroptosis and AMP-activated protein kinase (AMPK) signaling are important processes for ALL patients.
View Article and Find Full Text PDFAn Immunocytochemistry Method to Investigate the Translationally Active HIV Reservoir.
Int J Mol Sci
January 2025
MRL, Merck & Co., Inc., Rahway, NJ 07065, USA.
Despite the success of combination antiretroviral therapy (cART) to suppress HIV replication, HIV persists in a long-lived reservoir that can give rise to rebounding viremia upon cART cessation. The translationally active reservoir consists of HIV-infected cells that continue to produce viral proteins even in the presence of cART. These active reservoir cells are implicated in the resultant viremia upon cART cessation and likely contribute to chronic immune activation in people living with HIV (PLWH) on cART.
View Article and Find Full Text PDFSynthesis and preclinical evaluation of tigilanol tiglate analogs as latency-reversing agents for the eradication of HIV.
Sci Adv
January 2025
Department of Chemistry, Stanford University, Stanford, CA 94305, USA.
Tigilanol tiglate (EBC-46) is a selective modulator of protein kinase C (PKC) isoforms that is Food and Drug Administration (FDA) approved for the treatment of mast cell tumors in canines with up to an 88% cure rate. Recently, it has been FDA approved for the treatment of soft tissue sarcomas in humans. The role of EBC-46 and, especially, its analogs in efforts to eradicate HIV, treat neurological and cardiovascular disorders, or enhance antigen density in antigen-targeted chimeric antigen receptor-T cell and chimeric antigen receptor-natural killer cell immunotherapies has not been reported.
View Article and Find Full Text PDFAn artificial transcription factor that activates potent interferon-γ expression in human Jurkat T Cells.
Front Mol Med
January 2025
Department of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, United States.
Interferon (IFN)-γ is a central regulator of cell-mediated immunity in human health and disease, but reduced expression of the target receptors impairs signaling activity and leads to immunotherapy resistance. Although intracellular expression of IFN-γ restores the signaling and downstream functions, we lack the tools to activate the gene instead of cell surface receptors. This paper introduces the design and characterization of an artificial transcription factor (ATF) protein that recognizes the gene with six zinc finger domains, which are dovetailed to a VP64 signaling domain that promotes gene transcription and translation.
View Article and Find Full Text PDFWant 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!