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(3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis

  • Authors:
    • Ming‑Zhu Song
    • Feng‑Lin Zhang
    • Le‑Jun Lin
  • View Affiliations / Copyright

    Affiliations: Department of Orthopaedics and Traumatology, Yantaishan Hospital, Yantai, Shandong 264000, P.R. China, Department of Emergency, Yantai Hospital of Traditional Chinese Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, Shandong 264000, P.R. China, Department of Nuclear Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, Shandong 264000, P.R. China
    Copyright: © Song et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1107-1114
    |
    Published online on: June 18, 2019
       https://doi.org/10.3892/etm.2019.7681
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Abstract

As one of the leading causes of cancer‑associated mortalities worldwide, the overall survival rate of osteosarcoma has stably remained at 15‑30% for several decades. (3R)‑​5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one (TIM), isolated from the whole plant of Selaginella moellendorffii Hieron., has been reported to have pharmacological activities. In the present study, the anti‑proliferative effects of TIM against osteosarcoma were evaluated, and the underlying molecular mechanisms were explored. The results demonstrated that TIM inhibited proliferation and induced apoptosis in U2OS cells. Furthermore, the expression of the pro‑apoptotic protein NOXA in the intrinsic apoptosis pathway was upregulated by TIM, while the expression of myeloid cell leukemia 1, an anti‑apoptotic protein, was downregulated. In addition, TIM increased the protein expression of the endoplasmic reticulum stress markers inositol‑requiring enzyme 1, activating transcription factor 6 and glucose‑regulated protein 78. These results suggested that TIM induced ER stress response while activating intrinsic apoptosis. Furthermore, treating osteosarcoma tumor‑bearing mice with TIM significantly inhibited the tumor growth in the xenograft animal model. Overall, the study results suggested that TIM may serve as a potential antitumor agent against osteosarcoma.
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Copy and paste a formatted citation
Spandidos Publications style
Song MZ, Zhang FL and Lin LJ: (3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis. Exp Ther Med 18: 1107-1114, 2019.
APA
Song, M., Zhang, F., & Lin, L. (2019). (3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis. Experimental and Therapeutic Medicine, 18, 1107-1114. https://doi.org/10.3892/etm.2019.7681
MLA
Song, M., Zhang, F., Lin, L."(3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis". Experimental and Therapeutic Medicine 18.2 (2019): 1107-1114.
Chicago
Song, M., Zhang, F., Lin, L."(3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis". Experimental and Therapeutic Medicine 18, no. 2 (2019): 1107-1114. https://doi.org/10.3892/etm.2019.7681
Copy and paste a formatted citation
x
Spandidos Publications style
Song MZ, Zhang FL and Lin LJ: (3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis. Exp Ther Med 18: 1107-1114, 2019.
APA
Song, M., Zhang, F., & Lin, L. (2019). (3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis. Experimental and Therapeutic Medicine, 18, 1107-1114. https://doi.org/10.3892/etm.2019.7681
MLA
Song, M., Zhang, F., Lin, L."(3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis". Experimental and Therapeutic Medicine 18.2 (2019): 1107-1114.
Chicago
Song, M., Zhang, F., Lin, L."(3R)‑5,6,7‑trihydroxy‑3‑isopropyl‑3‑methylisochroman‑1‑one inhibited osteosarcoma growth by inducing apoptosis". Experimental and Therapeutic Medicine 18, no. 2 (2019): 1107-1114. https://doi.org/10.3892/etm.2019.7681
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