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Article

Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells

  • Authors:
    • Limeng Dai
    • Gang He
    • Kun Zhang
    • Xingying Guan
    • Yan Wang
    • Bo Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing 400038, P.R. China, Department of Pathogenic Biology, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing 400038, P.R. China
  • Pages: 660-667
    |
    Published online on: October 30, 2018
       https://doi.org/10.3892/ol.2018.9641
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Abstract

Trichostatin A (TSA) has been demonstrated to exhibit various anticancer effects that influence cell cycle arrest, cell proliferation and apoptosis of cancer cells. A potential association between TSA and endoplasmic reticulum (ER) function has been suggested but its anticancer mechanism involving the induction of ER stress is unknown. p53 has previously been demonstrated to regulate ER function in response to stress but its role involving TSA and ER stress in cancer cells is poorly understood. The current study identified that TSA induced ER stress in wild type (WT) HCT116 human colon cancer cells. Following TSA treatment, the ER stress markers GRP78 and GRP94 significantly increased without hyperacetylation of their promoter regions. The inositol‑requiring enzyme 1 α (IRE1α)/X‑box binding protein 1 (XBP1) pathway was implicated due to an association of phosphorylated IRE1α and spliced XBP1 with ER stress. However, luciferase reporter assay indicated that splicing events were attenuated in HCT116 TP53(‑/‑) cells. Furthermore, cell viability and apoptosis were revealed to depend on p53 during TSA treatment. Cell viability increased and the apoptosis rate decreased in HCT116 TP53(‑/‑) cells compared with WT HCT116 cells undergoing TSA treatment. In conclusion, the current study revealed that TSA may induce ER stress via a p53‑dependent mechanism in colon cancer cells. This provides information that may assist the development of treatments that exploit the anticancer function of TSA.
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Copy and paste a formatted citation
Spandidos Publications style
Dai L, He G, Zhang K, Guan X, Wang Y and Zhang B: Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells. Oncol Lett 17: 660-667, 2019.
APA
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., & Zhang, B. (2019). Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells. Oncology Letters, 17, 660-667. https://doi.org/10.3892/ol.2018.9641
MLA
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., Zhang, B."Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells". Oncology Letters 17.1 (2019): 660-667.
Chicago
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., Zhang, B."Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells". Oncology Letters 17, no. 1 (2019): 660-667. https://doi.org/10.3892/ol.2018.9641
Copy and paste a formatted citation
x
Spandidos Publications style
Dai L, He G, Zhang K, Guan X, Wang Y and Zhang B: Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells. Oncol Lett 17: 660-667, 2019.
APA
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., & Zhang, B. (2019). Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells. Oncology Letters, 17, 660-667. https://doi.org/10.3892/ol.2018.9641
MLA
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., Zhang, B."Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells". Oncology Letters 17.1 (2019): 660-667.
Chicago
Dai, L., He, G., Zhang, K., Guan, X., Wang, Y., Zhang, B."Trichostatin A induces p53‑dependent endoplasmic reticulum stress in human colon cancer cells". Oncology Letters 17, no. 1 (2019): 660-667. https://doi.org/10.3892/ol.2018.9641
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