Abstract
Platinum-based (especially cisplatin) chemotherapy is the main treatment after surgery for ovarian cancer. Although the initial treatment is effective, chemotherapy resistance develops rapidly. Therefore, chemotherapy resistance has always been a huge obstacle in the treatment of ovarian cancer. Staphylococcal nuclease domain-containing protein 1 (SND1) is an evolutionarily conserved multifunctional protein that plays a role in promoting tumorigenesis under various stress states. In this study, using MTT and SKOV3 ovarian cancer cells deficient in SND1 were observed to be more apoptotic and to express more apoptotic protein after treatment with cisplatin through the MTT, clone formation, and flow cytometry assays, while cells overexpressing SND1 exhibited a decreased number of apoptotic cells and expression of apoptotic proteins. Moreover, SND1 can regulate the expression of Growth arrest-specific 6 (GAS6) and then activate the AKT signaling pathway to achieve the regulation of sensitivity to cisplatin-induced apoptosis in ovarian cancer.
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Data availability
The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
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Acknowledgements
We would like to thank Prof. Lei Shi for kindly providing the lentivirus plasmids and the cell lines. This work was supported by the Science & Technology Development Fund of Tianjin Education Commission for Higher Education (2016YD18 to L. Xin).
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JY and LX contributed to the study conception and design. Material preparation, data collection, and analysis were performed by CH, LH, and YR. The first draft of the manuscript was written by LX and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.
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Ha, C., Hu, L., Ren, Y. et al. SND1 confers chemoresistance to cisplatin-induced apoptosis by targeting GAS6-AKT in SKOV3 ovarian cancer cells. Med Oncol 39, 169 (2022). https://doi.org/10.1007/s12032-022-01763-3
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DOI: https://doi.org/10.1007/s12032-022-01763-3