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Updated: Jun 15, 2026
Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
Published on: August 21, 2013
Atomic force microscope-related study membrane-associated cytotoxicity in human pterygium fibroblasts induced by
Xiaofang Cai1, Xiaoxi Yang, Jiye Cai
1Department of Chemistry, Jinan University, Guangzhou, Guangdong 510632, People's Republic of China.
Abstract:
Mitomycin C (MMC) has been shown to have a therapeutic effect against human pterygium fibroblasts (HPFs) by inducing apoptosis. However, there is little data about the effect of it on plasma membrane. In the present study, the cytotoxicity of MMC to HPFs including inhibiting cell growth, inducing apoptosis and bringing about membrane toxicity was investigated. It was found that MMC could significantly suppress the proliferation of HPFs in a dose-dependent manner by CCK-8 assay. Flow cytometric analysis also revealed that treatment with MMC resulted in increased percentages of apoptotic cells in a dose-dependent manner. Membrane lipid peroxidation level, lactate dehydrogenase (LDH) leakage, membrane surface topography, and membrane rigidity alterations were investigated to assess the membrane toxicity induced by MMC. Treatment with MMC at different concentrations accelerated membrane lipid peroxidation and potentiated LDH leakage, which was consistent with disturbance of membrane surface and decrease of membrane elasticity detected by atomic force microscopy. All the above changes led to the disturbed intracellular Ca(2+) homeostasis, which was an important signal triggering apoptosis. Hence, the membrane toxicity induced by MMC might play an important role in the process of apoptotic induction and the calcium channel may be one of the apoptosis mechanisms.
Insights
Mitomycin C (MMC) suppresses human pterygium fibroblast proliferation and induces apoptosis. MMC also causes plasma membrane damage, including lipid peroxidation and altered elasticity, contributing to cell death.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Mitomycin C (MMC) demonstrates therapeutic potential against human pterygium fibroblasts (HPFs) by inducing apoptosis.
- Limited data exists on MMC's specific effects on the plasma membrane of HPFs.
Purpose of the Study:
- To investigate the cytotoxicity of Mitomycin C (MMC) on human pterygium fibroblasts (HPFs).
- To elucidate the mechanisms of MMC-induced apoptosis, focusing on plasma membrane toxicity and calcium homeostasis.
Main Methods:
- Cell proliferation was assessed using the CCK-8 assay.
- Apoptosis was quantified via flow cytometry.
- Plasma membrane integrity was evaluated by measuring lipid peroxidation, lactate dehydrogenase (LDH) leakage, and atomic force microscopy (AFM) for surface topography and rigidity.
Main Results:
- MMC significantly inhibited HPF proliferation in a dose-dependent manner.
- MMC treatment increased apoptosis percentages in HPFs, also in a dose-dependent manner.
- MMC induced plasma membrane damage, evidenced by increased lipid peroxidation, LDH leakage, altered surface morphology, and reduced elasticity, leading to disturbed intracellular calcium homeostasis.
Conclusions:
- Mitomycin C exhibits dose-dependent cytotoxicity against HPFs, inhibiting proliferation and inducing apoptosis.
- MMC-induced plasma membrane toxicity plays a significant role in triggering apoptosis.
- Disruption of intracellular calcium homeostasis via calcium channels may be a key mechanism in MMC-induced apoptosis.
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