Abstract

Objective To study the mechanism of zoledronate (ZOL) triggering colorectal cancer cell line HCT116 apoptosis.Methods Flow cytometry detected the apoptosis of colorectal cancer cell line HCT116 treated by ZOL with 25 μmol/L or 50 μmol/L for 48 h; Fluorescent labeling and flow cytometry detected the JC-1 fluorescence changes in mitochondria; Western blotting analyzed the distribution of cytochrome C in mitochondria and cytosol.Results After 48 h of drug treatment,there was a significant apoptosis group in HCT116 cells [(11.6 ± 0.5) %,25 μmol/L; (49.2 ± 3.4) %,50 μmol/L; P < 0.01].The decreased fluorescence of JC-1 proved that the decreased mitochondrial membrane potential and dysfunction of mitochondria membrane [(96.49 ± 2.10)%,25 μmol/L,24 h; (86.13 ± 3.20)%,25 μ mol/L,48 h; (74.23 ± 5.30) %,25 μmol/L,72 h; P < 0.01].Meanwhile,Western blotting analysis showed that cytochrome C was decreased in mitochondria and increased in cytosol.It indicated that the cytochrome C was released from mitochondria after treatment with ZOL.Conclusion ZOL triggers HCTll6 colorectal cancer cell line apoptosis by mitochondria pathway. Key words: HCT116; Zoledronate; Mitochondria; Cytochrome C

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