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Article

MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy

  • Authors:
    • Xiangliang Zhang
    • Huijuan Shi
    • Shengqv Lin
    • Mingchen Ba
    • Shuzhong Cui
  • View Affiliations / Copyright

    Affiliations: Department of Abdominal Surgery (Section 2), The Affiliated Cancer Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510095, P.R. China, Department of Pathology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China
  • Pages: 1557-1564
    |
    Published online on: June 25, 2015
       https://doi.org/10.3892/or.2015.4078
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Abstract

Radioresistance has become a challenge in the treatment of pancreatic cancer, which limits the efficacy and outcomes of radiotherapy in clinical treatment. Autophagy, recognized as an adaptive response to cell stress, has recently been involved in the radioresistance of cancer cells. MicroRNAs (miRNAs) are also involved in the radioresistance of pancreatic cancer cells. In the present study, we established a radioresistant pancreatic cancer cell line and found that miRNA-216a was significantly downregulated whereas the autophagy activity was increased as compared with the control. Forced expression of miR-216a was found to inhibit the expression of beclin-1, a critical autophagic gene, as well as autophagy. Using bioinformatics analysis and the dual-luciferase reporter gene assay, we found that miR-216a directly interacted with 3'-untranslated region (UTR) of beclin-1. Furthermore, the forced expression of miR‑216a inhibited cell growth and colony formation ability and promoted the cell apoptosis of radioresistant pancreatic cancer cells in response to irradiation. By contrast, overexpression of beclin-1 abrogated the effects of miR-216a. Furthermore, miR-216a sensitized xenograft tumor to irradiation treatment and inhibited irradiation-induced autophagy by regulating beclin-1. Collectively, the results demonstrated that miR‑216a enhanced the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy, suggesting a promising molecular target for improving the radiotherapy of pancreatic cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang X, Shi H, Lin S, Ba M and Cui S: MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy. Oncol Rep 34: 1557-1564, 2015.
APA
Zhang, X., Shi, H., Lin, S., Ba, M., & Cui, S. (2015). MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy. Oncology Reports, 34, 1557-1564. https://doi.org/10.3892/or.2015.4078
MLA
Zhang, X., Shi, H., Lin, S., Ba, M., Cui, S."MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy". Oncology Reports 34.3 (2015): 1557-1564.
Chicago
Zhang, X., Shi, H., Lin, S., Ba, M., Cui, S."MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy". Oncology Reports 34, no. 3 (2015): 1557-1564. https://doi.org/10.3892/or.2015.4078
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang X, Shi H, Lin S, Ba M and Cui S: MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy. Oncol Rep 34: 1557-1564, 2015.
APA
Zhang, X., Shi, H., Lin, S., Ba, M., & Cui, S. (2015). MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy. Oncology Reports, 34, 1557-1564. https://doi.org/10.3892/or.2015.4078
MLA
Zhang, X., Shi, H., Lin, S., Ba, M., Cui, S."MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy". Oncology Reports 34.3 (2015): 1557-1564.
Chicago
Zhang, X., Shi, H., Lin, S., Ba, M., Cui, S."MicroRNA-216a enhances the radiosensitivity of pancreatic cancer cells by inhibiting beclin-1-mediated autophagy". Oncology Reports 34, no. 3 (2015): 1557-1564. https://doi.org/10.3892/or.2015.4078
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