Open Access

Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy

  • Authors:
    • Shuai Liu
    • Xin Li
    • Qing Li
    • Hongjun Liu
    • Yulong Shi
    • Hongqing Zhuo
    • Chensheng Li
    • Huijuan Zhu
  • View Affiliations

  • Published online on: March 16, 2018     https://doi.org/10.3892/ol.2018.8282
  • Pages: 7707-7715
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Colorectal cancer (CRC) is the third most common cause of cancer-associated mortality worldwide. Currently, 5-fluorouracil (5-FU) remains a widely used chemotherapeutic drug in the treatment of CRC; however, 5‑FU resistance during treatment has become a common problem. Livin, a member of the inhibitor of apoptosis protein family, is considered to be associated with tumor resistance to chemotherapy. In the present study, Livin‑silenced cells were generated by introducing a lentivirus into HCT116 and SW620 colon cancer cell lines. Acridine orange/ethidium bromide staining was used as an indicator of cell death. Western blot analysis was performed to detect protein expression levels, and transmission electron microscopy was used to assess autophagy. The half‑maximal inhibitory concentration of 5‑FU in colon cancer cells was evaluated using a Cell Counting Kit‑8 assay. The results of the present study confirmed that silencing Livin significantly enhanced colon cancer cell death in the presence of 5‑FU, increased expression levels of various apoptosis‑ and autophagy‑associated proteins and augmented chemotherapeutic sensitivity to 5‑FU. Furthermore, the present study demonstrated that this effect may be reversed when autophagy or apoptosis was inhibited, indicating that apoptosis and autophagy were involved in this process. The protein kinase B signaling pathway and B‑cell lymphoma‑2 expression levels significantly decreased following Livin knockdown, suggesting they may contribute to the regulation of apoptosis and autophagy crosstalk, which caused the Livin knockdown-induced cell death observed.
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May-2018
Volume 15 Issue 5

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

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Spandidos Publications style
Liu S, Li X, Li Q, Liu H, Shi Y, Zhuo H, Li C and Zhu H: Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy. Oncol Lett 15: 7707-7715, 2018
APA
Liu, S., Li, X., Li, Q., Liu, H., Shi, Y., Zhuo, H. ... Zhu, H. (2018). Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy. Oncology Letters, 15, 7707-7715. https://doi.org/10.3892/ol.2018.8282
MLA
Liu, S., Li, X., Li, Q., Liu, H., Shi, Y., Zhuo, H., Li, C., Zhu, H."Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy". Oncology Letters 15.5 (2018): 7707-7715.
Chicago
Liu, S., Li, X., Li, Q., Liu, H., Shi, Y., Zhuo, H., Li, C., Zhu, H."Silencing Livin improved the sensitivity of colon cancer cells to 5-fluorouracil by regulating crosstalk between apoptosis and autophagy". Oncology Letters 15, no. 5 (2018): 7707-7715. https://doi.org/10.3892/ol.2018.8282