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October-2015 Volume 12 Issue 4

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Article

Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways

  • Authors:
    • Zhen Huang
    • Ye Xu
    • Wei Peng
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, Shanghai Traditional Chinese Medicine‑Integrated Hospital, Shanghai 200082, P.R. China
  • Pages: 5939-5944
    |
    Published online on: August 12, 2015
       https://doi.org/10.3892/mmr.2015.4222
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Abstract

Colchicine is a natural compound, which belongs to the botanical family Colchicaceae and prevents growth of cancer cells via antimitotic activity by interacting with microtubules. Although numerous studies have demonstrated that the effect of colchicine on cell apoptosis is mediated by the activation of caspase‑3, the signaling pathways involved in the process remain unknown. In the current study, evidence is presented regarding the missing information using HT‑29 human colon cancer cells. The effect of colchicine on apoptosis in HT‑29 cells and the apoptosis‑associated signaling pathways were determined using various methods, including cell viability assay, Annexin V/propidium idodide (PI) binding, PI staining, Hoechst 33342 staining, mitochondrial membrane potential (Δψm) assay, reactive oxygen species (ROS) assay and western blot analysis. Colchicine was observed to induce a dose‑dependent reduction in cell viability in HT‑29 cells and early apoptosis occurred when the cells were treated with 1 µg/ml colchicine. Furthermore, colchicine treatment induced a loss of Δψm, increased ROS production, activated caspase‑3, upregulated BAX expression and downregulated Bcl‑2 expression, which evidenced the colchicine activity on apoptosis, potentially by acting via the intrinsic apoptotic signaling pathway. Colchicine increased phosphorylation of p38, although not phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase, which indicates that colchicine activates the p38 signaling pathway in order to induce cell apoptosis. Therefore, colchicine exhibited significant growth inhibition of the HT‑29 colon cancer cell line and induced apoptosis in the cells via the mitochondrial pathway, which is regulated by p38 signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Huang Z, Xu Y and Peng W: Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways. Mol Med Rep 12: 5939-5944, 2015.
APA
Huang, Z., Xu, Y., & Peng, W. (2015). Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways. Molecular Medicine Reports, 12, 5939-5944. https://doi.org/10.3892/mmr.2015.4222
MLA
Huang, Z., Xu, Y., Peng, W."Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways". Molecular Medicine Reports 12.4 (2015): 5939-5944.
Chicago
Huang, Z., Xu, Y., Peng, W."Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways". Molecular Medicine Reports 12, no. 4 (2015): 5939-5944. https://doi.org/10.3892/mmr.2015.4222
Copy and paste a formatted citation
x
Spandidos Publications style
Huang Z, Xu Y and Peng W: Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways. Mol Med Rep 12: 5939-5944, 2015.
APA
Huang, Z., Xu, Y., & Peng, W. (2015). Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways. Molecular Medicine Reports, 12, 5939-5944. https://doi.org/10.3892/mmr.2015.4222
MLA
Huang, Z., Xu, Y., Peng, W."Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways". Molecular Medicine Reports 12.4 (2015): 5939-5944.
Chicago
Huang, Z., Xu, Y., Peng, W."Colchicine induces apoptosis in HT‑29 human colon cancer cells via the AKT and c-Jun N-terminal kinase signaling pathways". Molecular Medicine Reports 12, no. 4 (2015): 5939-5944. https://doi.org/10.3892/mmr.2015.4222
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