Open Access

Effects of trans‑(±)‑kusunokinin on chemosensitive and chemoresistant ovarian cancer cells

  • Authors:
    • Nadeeya Mad-Adam
    • Thidarath Rattanaburee
    • Tanotnon Tanawattanasuntorn
    • Potchanapond Graidist
  • View Affiliations

  • Published online on: December 22, 2021     https://doi.org/10.3892/ol.2021.13177
  • Article Number: 59
  • Copyright: © Mad-Adam et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ovarian cancer ranks eighth in cancer incidence and mortality among women worldwide. Cisplatin‑based chemotherapy is commonly used for patients with ovarian cancer. However, the clinical efficacy of cisplatin is limited due to the occurrence of adverse side effects and development of cancer chemoresistance during treatment. Trans‑(±)‑kusunokinin has been previously reported to inhibit cell proliferation and induce cell apoptosis in various cancer cell types, including breast, colon and cholangiocarcinoma. However, the potential effects of (±)‑kusunokinin on ovarian cancer remains unknown. In the present study, chemosensitive ovarian cancer cell line A2780 and chemoresistant ovarian cancer cell lines A2780cis, SKOV‑3 and OVCAR‑3 were treated with trans‑(±)‑kusunokinin to investigate its potential effects. MTT, colony formation, apoptosis and multi‑caspase assays were used to determine cytotoxicity, the ability of single cells to form colonies, induction of apoptosis and multi‑caspase activity, respectively. Moreover, western blot analysis was performed to determine the proteins level of topoisomerase II, cyclin D1, CDK1, Bax and p53‑upregulated modulator of apoptosis (PUMA). The results demonstrated that trans‑(±)‑kusunokinin exhibited the strongest cytotoxicity against A2780cis cells with an IC50 value of 3.4 µM whilst also reducing the colony formation of A2780 and A2780cis cells. Trans‑(±)‑kusunokinin also induced the cells to undergo apoptosis and increased multi‑caspase activity in A2780 and A2780cis cells. This compound significantly downregulated topoisomerase II, cyclin D1 and CDK1 expression, but upregulated Bax and PUMA expression in both A2780 and A2780cis cells. In conclusion, trans‑(±)‑kusunokinin suppressed ovarian cancer cells through the inhibition of colony formation, cell proliferation and the induction of apoptosis. This pure compound could be a potential targeted therapy for ovarian cancer treatment in the future. However, studies in an animal model and clinical trial need to be performed to support the efficacy and safety of this new treatment.
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February-2022
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Spandidos Publications style
Mad-Adam N, Rattanaburee T, Tanawattanasuntorn T and Graidist P: Effects of trans‑(±)‑kusunokinin on chemosensitive and chemoresistant ovarian cancer cells. Oncol Lett 23: 59, 2022.
APA
Mad-Adam, N., Rattanaburee, T., Tanawattanasuntorn, T., & Graidist, P. (2022). Effects of trans‑(±)‑kusunokinin on chemosensitive and chemoresistant ovarian cancer cells. Oncology Letters, 23, 59. https://doi.org/10.3892/ol.2021.13177
MLA
Mad-Adam, N., Rattanaburee, T., Tanawattanasuntorn, T., Graidist, P."Effects of trans‑(±)‑kusunokinin on chemosensitive and chemoresistant ovarian cancer cells". Oncology Letters 23.2 (2022): 59.
Chicago
Mad-Adam, N., Rattanaburee, T., Tanawattanasuntorn, T., Graidist, P."Effects of trans‑(±)‑kusunokinin on chemosensitive and chemoresistant ovarian cancer cells". Oncology Letters 23, no. 2 (2022): 59. https://doi.org/10.3892/ol.2021.13177