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Article Open Access

Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells

  • Authors:
    • Yanjie Wei
    • Chenhao Li
    • Yuan Zhang
    • Hailan He
    • Guozhi Zhang
    • Xiaohui Hao
    • Heliang Liu
    • Hongli Wang
    • Wei Tian
  • View Affiliations / Copyright

    Affiliations: Medical Research Center, North China University of Science and Technology, Tangshan, Hebei 063000, P.R. China, Department of Oncology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China, Department of General Surgery, North China University of Science and Technology Affiliated Hospital, Tangshan, Hebei 063000, P.R. China
    Copyright: © Wei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 6322-6328
    |
    Published online on: February 22, 2018
       https://doi.org/10.3892/ol.2018.8107
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Abstract

Hydroxycamptothecin (HCPT) represents a new generation of anticancer drugs, with almost no side effects when used for the treatment of a number of types of cancer. Autophagy is becoming recognized as an important biological mechanism in human cancer, including lung cancer. However, the involvement of autophagy in the antiproliferative effects of HCPT on lung cancer remains unclear. In the present study, A549 cells, an accepted model of non‑small cell lung cancer (NSCLC) cells, were employed. It was demonstrated that HCPT was able to suppress proliferation and induce apoptosis and autophagy in A549 cells. The molecular mechanism underlying HCPT‑induced cell death was attributed to apoptosis and autophagy. Furthermore, it was demonstrated that an autophagy inhibitor, 3‑methyladenine, accelerated HCPT‑induced cell death in A549 cells. The results of the present study may lead to a deeper understanding of the molecular mechanism by which HCPT regulates NSCLC A549 cells. These results highlight the potential use of autophagy inhibitors in combination with traditional chemotherapy drugs for the treatment of lung cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Wei Y, Li C, Zhang Y, He H, Zhang G, Hao X, Liu H, Wang H and Tian W: Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells. Oncol Lett 15: 6322-6328, 2018.
APA
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X. ... Tian, W. (2018). Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells. Oncology Letters, 15, 6322-6328. https://doi.org/10.3892/ol.2018.8107
MLA
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X., Liu, H., Wang, H., Tian, W."Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells". Oncology Letters 15.5 (2018): 6322-6328.
Chicago
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X., Liu, H., Wang, H., Tian, W."Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells". Oncology Letters 15, no. 5 (2018): 6322-6328. https://doi.org/10.3892/ol.2018.8107
Copy and paste a formatted citation
x
Spandidos Publications style
Wei Y, Li C, Zhang Y, He H, Zhang G, Hao X, Liu H, Wang H and Tian W: Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells. Oncol Lett 15: 6322-6328, 2018.
APA
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X. ... Tian, W. (2018). Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells. Oncology Letters, 15, 6322-6328. https://doi.org/10.3892/ol.2018.8107
MLA
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X., Liu, H., Wang, H., Tian, W."Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells". Oncology Letters 15.5 (2018): 6322-6328.
Chicago
Wei, Y., Li, C., Zhang, Y., He, H., Zhang, G., Hao, X., Liu, H., Wang, H., Tian, W."Hydroxycamptothecin mediates antiproliferative effects through apoptosis and autophagy in A549 cells". Oncology Letters 15, no. 5 (2018): 6322-6328. https://doi.org/10.3892/ol.2018.8107
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