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Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line

  • Authors:
    • Jilan Liu
    • Xianyun Qin
    • Wenyuan Ma
    • Shu Jia
    • Xiaobei Zhang
    • Xinlin Yang
    • Dongfeng Pan
    • Feng Jin
  • View Affiliations / Copyright

    Affiliations: Department of Central Laboratory, Affiliated Hospital of Jining Medical University, Jining, Shandong 272029, P.R. China, Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining, Shandong 272029, P.R. China, Department of Orthopaedic Surgery, Orthopaedic Research Labs, University of Virginia, Charlottesville, VA 22908, USA, Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, VA 22908, USA
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 320
    |
    Published online on: March 5, 2021
       https://doi.org/10.3892/mmr.2021.11959
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Abstract

Corilagin, extracted from the Euphorbiaceae and Phyllanthus plants, inhibits the growth of a number of types of tumors. Compared with temozolomide, the traditional chemotherapy drug, corilagin has demonstrated stronger antitumor activity. However, the pharmaceutical mechanism of corilagin in glioma remains unclear. Nuclear factor erythroid 2 like 2 (NFE2L2 or NRF2) is positively associated with several types of tumor including glioma. In the present study, NRF2 expression was higher in glioma tissues compared with non‑glioma specimens. Therefore, it was hypothesized that corilagin targets NRF2 regulation of U251 cell apoptosis. The present study used Hoechst 33258 staining to demonstrate that corilagin induced glioma cell apoptosis and observed that the expression of the apoptosis‑related gene Bcl‑2 was reduced. In addition, corilagin induced autophagy and promoted the conversion of light chain 3 (LC3) protein from LC3Ⅰ to LC3II. NRF2 expression was downregulated by corilagin stimulation. Furthermore, the gene expression pattern following knockdown of NRF2 in U251 cells using siRNA was consistent with corilagin stimulation. Therefore, it was preliminarily concluded that corilagin induces apoptosis and autophagy by reducing NRF2 expression.
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Copy and paste a formatted citation
Spandidos Publications style
Liu J, Qin X, Ma W, Jia S, Zhang X, Yang X, Pan D and Jin F: Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line. Mol Med Rep 23: 320, 2021.
APA
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X. ... Jin, F. (2021). Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line. Molecular Medicine Reports, 23, 320. https://doi.org/10.3892/mmr.2021.11959
MLA
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X., Pan, D., Jin, F."Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line". Molecular Medicine Reports 23.5 (2021): 320.
Chicago
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X., Pan, D., Jin, F."Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line". Molecular Medicine Reports 23, no. 5 (2021): 320. https://doi.org/10.3892/mmr.2021.11959
Copy and paste a formatted citation
x
Spandidos Publications style
Liu J, Qin X, Ma W, Jia S, Zhang X, Yang X, Pan D and Jin F: Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line. Mol Med Rep 23: 320, 2021.
APA
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X. ... Jin, F. (2021). Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line. Molecular Medicine Reports, 23, 320. https://doi.org/10.3892/mmr.2021.11959
MLA
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X., Pan, D., Jin, F."Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line". Molecular Medicine Reports 23.5 (2021): 320.
Chicago
Liu, J., Qin, X., Ma, W., Jia, S., Zhang, X., Yang, X., Pan, D., Jin, F."Corilagin induces apoptosis and autophagy in NRF2‑addicted U251 glioma cell line". Molecular Medicine Reports 23, no. 5 (2021): 320. https://doi.org/10.3892/mmr.2021.11959
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