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Article

Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation

  • Authors:
    • Xian-Ling Guo
    • Fei Hu
    • Hui Wang
    • Jue-Min Fang
    • Zhong-Ζheng Zhu
    • Li-Χin Wei
    • Qing Xu
  • View Affiliations / Copyright

    Affiliations: Department of Medical Oncology, Dermatology Hospital, Tongji University, Shanghai 200072, P.R. China, Department of Medical Oncology, 10th People's Hospital, Tongji University, Shanghai 200072, P.R. China, Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai 200438, P.R. China
  • Pages: 773-783
    |
    Published online on: November 27, 2017
       https://doi.org/10.3892/or.2017.6115
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Abstract

Autophagy is a lysosome-dependent process involved in protein and organelle degradation. It has been suggested that autophagy is activated in nutrient-deficient condition and plays an important role in protecting cells from nutrient shortage. However, the effect of autophagy on chemotherapy during nutrient deficiency has been rarely researched. In the present study, we discovered that hepatocarcinoma cells exhibit chemoinsensitivity accompanied by the activation of autophagy when cultured in nutrient-deprived medium. Inhibition of autophagy by 3-methyladenine or siRNA‑targeted Beclin 1 increased the nutrient deprivation‑induced apoptosis and chemosensitivity in hepatocarcinoma cells. Furthermore, decreased mitochondrial mass was detected when cells underwent autophagy. The present study suggests that induction of autophagy confers a survival advantage for hepatocarcinoma cells during nutrient deprivation, not only rescuing cells from nutrient deficiency-induced cell apoptosis, but also protecting cells from chemotherapy-induced cell death. Combined usage of the inhibition of autophagy and conventional chemotherapeutic agents could be an effective therapy for hepatocarcinoma during nutrient deprivation.
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Copy and paste a formatted citation
Spandidos Publications style
Guo X, Hu F, Wang H, Fang J, Zhu Z, Wei L and Xu Q: Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation. Oncol Rep 39: 773-783, 2018.
APA
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., & Xu, Q. (2018). Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation. Oncology Reports, 39, 773-783. https://doi.org/10.3892/or.2017.6115
MLA
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., Xu, Q."Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation". Oncology Reports 39.2 (2018): 773-783.
Chicago
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., Xu, Q."Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation". Oncology Reports 39, no. 2 (2018): 773-783. https://doi.org/10.3892/or.2017.6115
Copy and paste a formatted citation
x
Spandidos Publications style
Guo X, Hu F, Wang H, Fang J, Zhu Z, Wei L and Xu Q: Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation. Oncol Rep 39: 773-783, 2018.
APA
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., & Xu, Q. (2018). Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation. Oncology Reports, 39, 773-783. https://doi.org/10.3892/or.2017.6115
MLA
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., Xu, Q."Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation". Oncology Reports 39.2 (2018): 773-783.
Chicago
Guo, X., Hu, F., Wang, H., Fang, J., Zhu, Z., Wei, L., Xu, Q."Inhibition of autophagy in hepatocarcinoma cells promotes chemotherapeutic agent-induced apoptosis during nutrient deprivation". Oncology Reports 39, no. 2 (2018): 773-783. https://doi.org/10.3892/or.2017.6115
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