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Article Open Access

Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling

  • Authors:
    • Weiwei Han
    • Wenjing Xing
    • Kechao Wang
    • Benjun Wang
    • Keyun Bai
  • View Affiliations / Copyright

    Affiliations: Department of Anorectal, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250014, P.R. China, Department of Traditional Chinese Medicine, Zibo Central Hospital, Zibo, Shandong 255000, P.R. China
    Copyright: © Han et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 249
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    Published online on: June 7, 2022
       https://doi.org/10.3892/ol.2022.13369
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Abstract

Despite the advancement in the diagnosis and therapeutic strategies for colorectal cancer, the outcomes of patients with colorectal cancer remain unsatisfactory. Alisol A is a natural constituent of Alismatis rhizoma (zexie) and has demonstrated anti‑cancer properties; however, the function of Alisol A in colorectal cancer is still unknown. In the present study, the effect of Alisol A on colorectal cancer progression was investigated. MTT and colony formation assays showed that treatment with Alisol A repressed colorectal cancer cell proliferation in a dose‑dependent manner. Similarly, western blot analysis demonstrated that Alisol A upregulated E‑cadherin protein expression levels, but downregulated N‑cadherin and Vimentin protein expression levels in colorectal cancer cells. In addition, the number of cells in G0/G1 phase was enhanced, while that of S phase was reduced in Alisol A‑treated colorectal cancer cells. Apoptosis and pyroptosis of colorectal cancer cells were stimulated following treatment with Alisol A. Alisol A suppressed the migration ability of colorectal cancer cells in a dose‑dependent manner. Moreover, Alisol A increased the chemotherapeutic sensitivity of colorectal cancer cells to cisplatin. Mechanically, western blot analysis confirmed that Alisol A repressed the phosphorylation levels of PI3K, Akt and mTOR in colorectal cancer cells. The Akt activator, SC79 reversed the effect of Alisol A on colorectal cancer cell proliferation and apoptosis. In conclusion, Alisol A induced an inhibitory effect on colorectal cancer progression by inactivating PI3K/Akt signaling.
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Copy and paste a formatted citation
Spandidos Publications style
Han W, Xing W, Wang K, Wang B and Bai K: Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling. Oncol Lett 24: 249, 2022.
APA
Han, W., Xing, W., Wang, K., Wang, B., & Bai, K. (2022). Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling. Oncology Letters, 24, 249. https://doi.org/10.3892/ol.2022.13369
MLA
Han, W., Xing, W., Wang, K., Wang, B., Bai, K."Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling". Oncology Letters 24.2 (2022): 249.
Chicago
Han, W., Xing, W., Wang, K., Wang, B., Bai, K."Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling". Oncology Letters 24, no. 2 (2022): 249. https://doi.org/10.3892/ol.2022.13369
Copy and paste a formatted citation
x
Spandidos Publications style
Han W, Xing W, Wang K, Wang B and Bai K: Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling. Oncol Lett 24: 249, 2022.
APA
Han, W., Xing, W., Wang, K., Wang, B., & Bai, K. (2022). Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling. Oncology Letters, 24, 249. https://doi.org/10.3892/ol.2022.13369
MLA
Han, W., Xing, W., Wang, K., Wang, B., Bai, K."Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling". Oncology Letters 24.2 (2022): 249.
Chicago
Han, W., Xing, W., Wang, K., Wang, B., Bai, K."Alisol A attenuates malignant phenotypes of colorectal cancer cells by inactivating PI3K/Akt signaling". Oncology Letters 24, no. 2 (2022): 249. https://doi.org/10.3892/ol.2022.13369
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