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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/14918
Title: Death receptor-dependent apoptosis and cell cycle delay induced by bioymifi in human cervical cancer cells
Authors: Altun, Ahmet
Şahin Inan, Zeynep Deniz
Yulak, Fatih
Keywords: Apoptosis
bioymifi, cell cycle
cervical cancer
death receptor
Issue Date: 20-Jul-2022
Publisher: Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi.
Citation: Altun, A., Inan, Z. D. Ş., & Yulak, F. (2022). Death receptor-dependent apoptosis and cell cycle delay induced by bioymifi in human cervical cancer cells. Pakistan Journal of Pharmaceutical Sciences, 35(4).
Abstract: In chemotherapy applied against cervical cancer, non-specific cytotoxicity and drug resistance that develops over time are trying to be overcome. Therefore, the development of effective and innovative chemotherapeutic drugs for the treatment is among the priority issues in the medical field. The anticancer activity of the Bioymifi, which can activate apoptosis by inducing DR-5 clustering and aggregation against the human cervical cancer cell line, was investigated in the current study. The cytotoxic activity of Bioymifi on the HeLa cell line was identified using XTT assay. The pathway of the cell death mechanism was analyzed through the cell cycle and Annexin V assays by the flow cytometry. DAPI staining assay was applied under fluorescence microscopy to examine the nuclear morphology. Bioymifi appeared to have a remarkable IC50 value (11.75μM) against HeLa cells. The cell cycle analysis demonstrated the increase of Bioymifi cured HeLa cells in the S phase. And also, 11.75µM of Bioymifi caused a significantly higher apoptotic effect compared to control. In addition, in vitro immunofluorescence experiments of this study represented that Bioymifi reduced Ki-67 localization in HeLa cells. Bioymifi has significantly anticancer actions in Human cervix cancer in vitro and can be combined with standard treatment.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/14918
ISSN: 1011-601X
Appears in Collections:Issue No.4

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