Echinophora platyloba DC (Apiaceae) crude extract induces apoptosis in human prostate adenocarcinoma cells (PC 3)
Fatemeh Zare Shahneh, Behzad Baradaran1, Jafar Majidi
1Immunology Research Center; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Science, Tabriz, Iran.
Background:
Prostate cancer is the second leading malignancy worldwide and the second prominent cause of cancer-related deaths among men. Therefore, there is a serious necessity for finding advanced alternative therapeutic measures against this lethal malignancy. In this article, we report the cytotoxicity and the mechanism of cell death of the methanolic extract prepared from Echinophora platyloba DC plant against human prostate adenocarcinoma PC 3 cell line and Human Umbilical Vein Endothelial Cells HUVEC cell line.
Methods:
Cytotoxicity and viability of the methanolic extract were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and dye exclusion assay. Cell death enzyme-linked immunosorbent assay (ELISA) was employed to quantify the nucleosome production resulting from nuclear DNA fragmentation during apoptosis and determine whether the mechanism involves induction of apoptosis or necrosis. The cell death was identified as apoptosis using terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay and DNA fragmentation gel electrophoresis.
Results:
E. platyloba could decrease cell viability in malignant cells in a dose- and time-dependent manner. The IC50 values against PC 3 were determined as 236.136 ± 12.4, 143.400 ± 7.2, and 69.383 ± 1.29 μg/ml after 24, 36, and 48 h, respectively, but there was no significant activity in HUVEC normal cell (IC50 > 800 μg/ml). Morphological characterizations and DNA laddering assay showed that the methanolic extract treated cells displayed marked apoptotic characteristics such as nuclear fragmentation, appearance of apoptotic bodies, and DNA laddering fragment. Increase in an early apoptotic population was observed in a dose-dependent manner. PC 3 cell death elicited by the extract was found to be apoptotic in nature based a clear indication of TUNEL assay and gel electrophoresis DNA fragmentation, which is a hallmark of apoptosis.
Conclusions:
In summary, the E. platyloba extract attenuated the human prostate adenocarcinoma cell proliferation in vitro possibly by inducing apoptosis. E. platyloba is likely to be valuable for the treatment of human prostate adenocarcinoma.
Insights
The Echinophora platyloba plant extract shows promise as a natural treatment for prostate cancer by inducing apoptosis in cancer cells. This study demonstrates its effectiveness against prostate adenocarcinoma cells while sparing normal cells.
Area of Science:
- Phytochemistry
- Cancer Biology
- Pharmacology
Background:
- Prostate cancer is a leading cause of cancer-related deaths in men globally.
- There is a critical need for novel therapeutic strategies against this malignancy.
- This study investigates the anti-cancer properties of Echinophora platyloba.
Purpose of the Study:
- To evaluate the cytotoxicity of Echinophora platyloba methanolic extract on prostate cancer cells (PC-3) and normal endothelial cells (HUVEC).
- To elucidate the mechanism of cell death induced by the extract.
Main Methods:
- Cytotoxicity assessed using MTT and dye exclusion assays.
- Apoptosis induction confirmed via TUNEL assay, DNA fragmentation, and morphological analysis.
- Cell death mechanism differentiated between apoptosis and necrosis using ELISA.
Main Results:
- The extract exhibited dose- and time-dependent cytotoxicity against PC-3 cells with specific IC50 values at different time points.
- No significant cytotoxicity was observed in normal HUVEC cells (IC50 > 800 μg/ml).
- Morphological and molecular analyses confirmed apoptosis as the primary mechanism of cell death.
Conclusions:
- Echinophora platyloba extract effectively inhibits prostate adenocarcinoma cell proliferation in vitro.
- The extract induces apoptosis in cancer cells, suggesting its potential as a therapeutic agent for prostate cancer.
