Abstract
Natural products have a significant role in the development of new drugs, being relevant the pentacyclic triterpenes extracted from Olea europaea L. Anticancer effect of uvaol, a natural triterpene, has been scarcely studied. The aim of this study was to understand the anticancer mechanism of uvaol in the HepG2 cell line. Cytotoxicity results showed a selectivity effect of uvaol with higher influence in HepG2 than WRL68 cells used as control. Our results show that uvaol has a clear and selective anticancer activity in HepG2 cells supported by a significant anti-migratory capacity and a significant increase in the expression of HSP-60. Furthermore, the administration of this triterpene induces cell arrest in the G0/G1 phase, as well as an increase in the rate of cell apoptosis. These results are supported by a decrease in the expression of the anti-apoptotic protein Bcl2, an increase in the expression of the pro-apoptotic protein Bax, together with a down-regulation of the AKT/PI3K signaling pathway. A reduction in reactive oxygen species (ROS) levels in HepG2 cells was also observed. Altogether, results showed anti-proliferative and pro-apoptotic effect of uvaol on hepatocellular carcinoma, constituting an interesting challenge in the development of new treatments against this type of cancer.
Highlights
Cancer is one of the leading causes of mortality worldwide, especially in developed countries, on account of the aging of the population [1]
Referring to the WRL68 line, we can observe that its growth on the support is morphology at 10 magnifications
The results show the percentage of cells in each situation studied that express reactive oxygen species (ROS) (ROS+) and those that do not express them (ROS−)
Summary
Cancer is one of the leading causes of mortality worldwide, especially in developed countries, on account of the aging of the population [1]. Hepatocarcinogenesis is a process initiated by different external stimuli that induce genetic changes in hepatocytes or hepatic stem cells, which can cause alterations in the processes of proliferation and apoptosis, by dysfunctions in the cell cycle and its regulation, which eventually lead to tissue dysplasia and can cause a neoplasm [3]. In response to this DNA damage, different control points can be activated throughout the cell cycle phases. It is known that p53 is frequently mutated in HCC, disrupting the correct role of this protein [6]
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