Piperine acts as an anticancer agent by reducing cyclooxygenase-2 activity and inducing apoptosis by activating p53 in HeLa cells

Abstract

Cervical cancer is a malignant disease with the highest incidence in women worldwide. Human papillomavirus (HPV) infection causes cancer through degradation and decreased activity of the p53 gene, which is a significant contributor to the apoptosis pathway and a major factor in cancer incidence. In addition to p53, the cyclooxygenase-2 (COX-2) enzyme is essential for tumor formation via inflammatory pathways, particularly in cervical cancer caused by persistent HPV infection. This study aims to investigate how piperine treatment affects the HeLa cervical cancer cell line p53 expression, COX-2 levels, and cell proliferation. HeLa cells were divided into treated groups (65 and 130 μg/mL) and an untreated group as a control group. Its activity on COX-2 levels was further analyzed using the ELISA method and gene expression using the Livak qPCR method. Cell proliferation can be inhibited by piperine, with an IC₅₀ value of 66.68 μg/ml. Piperine can also increase p53 gene expression and suppress COX-2 levels in HeLa cells. Piperine has cell growth inhibitory activity, suppresses the inflammatory process by reducing COX-2 enzyme levels, and induces apoptosis through upregulation of the p53 gene.