Open Access

Effects and mechanism of STAT3 silencing on the growth and apoptosis of colorectal cancer cells

  • Authors:
    • Jing Li
    • You‑Yu Liu
    • Xue‑Feng Yang
    • Dao‑Fu Shen
    • Hong‑Zhi Sun
    • Ke‑Qiang Huang
    • Hua‑Chuan Zheng
  • View Affiliations

  • Published online on: August 29, 2018     https://doi.org/10.3892/ol.2018.9368
  • Pages: 5575-5582
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Signal transducer and activator of transcription 3 (STAT3) have roles in various cellular processes, including angiogenesis, apoptosis, cell cycle progression, cell migration and drug resistance. To clarify the effects of STAT3 in colorectal cancer (CRC) cells and the underlying molecular mechanisms, STAT3 was directly silenced, and the effects of STAT3 silencing on cell proliferation, apoptosis and growth with phenotype‑associated molecules were examined.pSH1‑Si‑STAT3 was successfully transfected into the CRC HCT‑116 and SW480 cell lines, which was verified by GFP tagging under a fluorescence microscope. An MTT assay revealed that the proliferation of both cell lines that were transfected with pSH1‑Si‑STAT3 was significantly suppressed in comparison with the control and mock (P<0.05). Acridine orange/ethidium bromide staining and flow cytometry indicated that the transfected cell lines had a significantly higher rate of apoptosis than the control‑ and mock‑treated cells (P<0.05). STAT3‑silienced cells were also significantly arrested at the G2/M stage compared with the cells that were transfected with control and mock plasmids (P<0.05). At the mRNA level, the expression of STAT3 and survivin was significantly downregulated (P<0.05), but p53 and caspase‑3 were significantly upregulated (P<0.05). The significantly different patterns of expression were observed in western blot analysis (P<0.05). The findings of the present study indicate that STAT3 silencing may suppress the proliferation and growth of CRC cells, and induce their apoptosis by upregulating the expression of survivin, p53 and caspase‑3. Therefore, STAT3 may be a good candidate for CRC gene therapy.
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November-2018
Volume 16 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Li J, Liu YY, Yang XF, Shen DF, Sun HZ, Huang KQ and Zheng HC: Effects and mechanism of STAT3 silencing on the growth and apoptosis of colorectal cancer cells. Oncol Lett 16: 5575-5582, 2018
APA
Li, J., Liu, Y., Yang, X., Shen, D., Sun, H., Huang, K., & Zheng, H. (2018). Effects and mechanism of STAT3 silencing on the growth and apoptosis of colorectal cancer cells. Oncology Letters, 16, 5575-5582. https://doi.org/10.3892/ol.2018.9368
MLA
Li, J., Liu, Y., Yang, X., Shen, D., Sun, H., Huang, K., Zheng, H."Effects and mechanism of STAT3 silencing on the growth and apoptosis of colorectal cancer cells". Oncology Letters 16.5 (2018): 5575-5582.
Chicago
Li, J., Liu, Y., Yang, X., Shen, D., Sun, H., Huang, K., Zheng, H."Effects and mechanism of STAT3 silencing on the growth and apoptosis of colorectal cancer cells". Oncology Letters 16, no. 5 (2018): 5575-5582. https://doi.org/10.3892/ol.2018.9368