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Olive: A Potential Suppressor for Cervical Cancer by Upregulation of P21

Background Cervical cancer is the second deadliest for women between the ages of 20 and 39 years. Even with prevention tactics for screening, incident rates and mortality of cervical cancer remain high. Olive has been shown to have many beneficial effects in humans concerning cardiovascular disease...

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Detalles Bibliográficos
Autores principales: Patel, Love, Deng, Zuliang, Zhu, Ziwen, Lequio, Marco, Hough, Jacob, Xiao, Huaping, Bai, Qian, Wakefiel, Mark R, Fang, Yujiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10246731/
https://www.ncbi.nlm.nih.gov/pubmed/37292535
http://dx.doi.org/10.7759/cureus.38719
Descripción
Sumario:Background Cervical cancer is the second deadliest for women between the ages of 20 and 39 years. Even with prevention tactics for screening, incident rates and mortality of cervical cancer remain high. Olive has been shown to have many beneficial effects in humans concerning cardiovascular disease and inflammation. Despite these promising benefits, little is known about its effect on cervical cancer. This study examined the effects and mechanism of effects of olive extract (OE) on the HeLa cervical cancer cell line. Methodology We utilized clonogenic survival assay, quick cell proliferation assay, and caspase-3 activity to investigate the effect of OE on the proliferation and apoptosis of the cervical cancer cell line HeLa. To investigate the mechanisms behind these findings, Reverse transcription polymerase chain reaction and immunohistochemistry were performed. Results OE inhibited the growth and proliferation of HeLa cells. In comparison to the control, the percentage of colonies, as well as the optical density of the cervical cancer cells, was found to be decreased. In addition, the relative activity of caspase-3, a marker for apoptosis, was increased after treatment with OE. The anti-proliferative effect of OE on HeLa cells correlated with the increase of an anti-proliferative molecule p21. However, the pro-apoptotic effect of OE was not correlated with the change in major pro-apoptotic or anti-apoptotic molecules examined in this study. Conclusions Our study suggests that OE inhibits the growth of HeLa cervical cancer cells by upregulation of p21. Further investigation of the effects of OE on cervical cancer and other cancers is warranted by these results.