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Induction of apoptosis in KB cells by pingyangmycin
1Department of Oral and Maxillofacial Surgery, Chung Shan Medical and Dental College Hospital, Taichung, Taiwan, ROC.
Abstract:
Pingyangmycin (PYM; Bleomycin A(5)), an antitumour antibiotic is currently used during anticancer therapy. Previous experiments demonstrated that the therapeutic efficiency of PYM for treatment of malignant tumours is considered to be related to its ability to cause DNA strand breaks in vitro. However, very little is known about the interaction of PYM with the target cells, and it is still unclear how PYM enters the cells. In this study, cell death induced by PYM was studied in a human squamous cell carcinoma cell line (KB cells). In order to determine if cell death occurred by necrosis (reproductive cell death) or apoptosis (programmed cell death), KB cells were exposed to different concentrations of PYM and evaluated by biochemical and morphological criteria. Our results indicate that KB cells displayed an arrest in the G(2)-M phase of the cell cycle and became enlarged and polynucleated before dying at the low concentrations of PYM. In contrast, when cells were exposed to high concentrations of PYM, morphological changes identical to those usually associated with apoptosis were observed as well as internucleosomal digestion of genomic DNA. In conclusion, we demonstrate that PYM is able to induce two distinct modes of cell death depending on the doses of PYM.
Insights
Pingyangmycin (PYM) induces distinct cell death modes in cancer cells. Low PYM concentrations cause G2-M arrest and cell enlargement, while high concentrations trigger apoptosis and DNA fragmentation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Pingyangmycin (PYM), an antitumour antibiotic, is used in anticancer therapy.
- PYM's efficacy is linked to its ability to induce DNA strand breaks.
- The precise mechanisms of PYM's cellular interaction and entry remain unclear.
Purpose of the Study:
- To investigate the cell death mechanisms induced by Pingyangmycin (PYM) in human squamous cell carcinoma KB cells.
- To differentiate between necrosis and apoptosis as modes of cell death caused by PYM.
Main Methods:
- KB cells were exposed to varying concentrations of PYM.
- Cell death was evaluated using biochemical and morphological criteria.
- Cell cycle progression was analyzed to identify specific phases of arrest.
Main Results:
- Low PYM concentrations induced G2-M cell cycle arrest, leading to enlarged and polynucleated cells.
- High PYM concentrations resulted in morphological changes characteristic of apoptosis.
- Internucleosomal digestion of genomic DNA was observed at high PYM concentrations, confirming apoptosis.
Conclusions:
- Pingyangmycin (PYM) induces distinct cell death pathways in KB cells.
- The mode of cell death is dose-dependent, with low doses causing G2-M arrest and high doses inducing apoptosis.