Open Access

Tumor necrosis factor‑related apoptosis‑inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway

  • Authors:
    • Hongyan Gong
    • Weicai Cheng
    • Yong Wang
  • View Affiliations

  • Published online on: October 30, 2018     https://doi.org/10.3892/etm.2018.6901
  • Pages: 41-50
  • Copyright: © Gong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Colon cancer is one of the most common types of gastrointestinal tumor. Previous studies have demonstrated that tumor necrosis factor‑(TNF)‑related apoptosis‑inducing ligand (TRAIL) reduces the aggressiveness of colon cancer tumors and promotes the apoptosis of colon carcinoma cells. In the present study, the inhibitory effects of TRAIL were investigated and the potential mechanism of TRAIL‑mediated apoptosis was explored in colon cancer cells. Reverse transcription‑quantitative polymerase chain reaction, western blotting, immunofluorescence, immunohistochemistry, TUNEL and flow cytometry assays were used to analyze the effects of TRAIL on the growth, migration, invasion and apoptosis of colon tumor cells. In vivo experiments were performed in mice to analyze the therapeutic effects of TRAIL. The results demonstrated that TRAIL significantly suppressed the growth of colorectal tumor cells in a dose‑dependent manner (0.5‑2.5 mg/ml) and also promoted colon tumor cell death. The migration and invasion of colon tumor cells were inhibited by the downregulation of fibronectin, Vimentin and E‑cadherin. The apoptotic rate revealed that TRAIL (2.0 mg/ml) significantly promoted the apoptosis of colon tumor cells by regulating apoptosis‑related gene expression. TRAIL administration promoted the apoptosis of colon tumor cells via the exogenous apoptosis signaling pathway due to the upregulation of caspase‑3, caspase‑8 and nuclear factor‑κB protein expression. In vivo assays revealed that TRAIL administration significantly inhibited tumor growth and promoted apoptotic body and lymphocyte infiltration, which led to increased survival in tumor‑bearing mice compared with the control group. Immunohistochemistry revealed that P53 and B‑cell lymphoma‑2 were downregulated in TRAIL‑treated tumors. In conclusion, TRAIL treatment significantly inhibited the growth and aggressiveness of colon tumors by inducing apoptosis via the exogenous apoptosis pathway, which suggests that TRAIL may be a potential anticancer agent for colon carcinoma therapy.
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January-2019
Volume 17 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Gong H, Cheng W and Wang Y: Tumor necrosis factor‑related apoptosis‑inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway. Exp Ther Med 17: 41-50, 2019
APA
Gong, H., Cheng, W., & Wang, Y. (2019). Tumor necrosis factor‑related apoptosis‑inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway. Experimental and Therapeutic Medicine, 17, 41-50. https://doi.org/10.3892/etm.2018.6901
MLA
Gong, H., Cheng, W., Wang, Y."Tumor necrosis factor‑related apoptosis‑inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway". Experimental and Therapeutic Medicine 17.1 (2019): 41-50.
Chicago
Gong, H., Cheng, W., Wang, Y."Tumor necrosis factor‑related apoptosis‑inducing ligand inhibits the growth and aggressiveness of colon carcinoma via the exogenous apoptosis signaling pathway". Experimental and Therapeutic Medicine 17, no. 1 (2019): 41-50. https://doi.org/10.3892/etm.2018.6901