Vernonia amygdalina Delile Induces Apoptotic Effects of PC3 Cells: Implication in the Prevention of Prostate Cancer

扁桃斑鸠菊诱导 PC3 细胞凋亡:对前列腺癌预防的意义

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作者:Clement G Yedjou, William Johnson, Solange S Tchounwou, Shaloam Dasari, Sylvianne Njiki, Paul B Tchounwou

Background

Prostate cancer (PCa) is one of the common cancers in males and its incidence keeps increasing globally. Approximately 81% of PCa is diagnosed during the early stage of the disease. The treatment options for prostate care include surgery, radiotherapy, and chemotherapy, but these treatments often have side effects that may lead to issues such as impotence or decreased bowel function. Our central goal is to test the apoptotic effects of Vernonia amygdalina Delile (an edible medicinal plant that is relatively inexpensive, nontoxic, and virtually without side effects) for the prevention of PCa using human adenocarcinoma (PC-3) cells as a test model.

Conclusions

These results suggest that inhibition of cancer cell growth, induction of cell cycle arrest, and apoptosis through caspase-3 activation and nucleosomal DNA fragmentation are involved in the therapeutic mechanisms of VAD as a candidate drug towards the prevention and/or treatment of PCa.

Methods

To address our central goal, PC-3 cells were treated with Vernonia amygdalina Delile (VAD). Cell cycle arrest and cell apoptosis were evaluated by Flow Cytometry assessment. Nucleosomal DNA fragmentation was detected by agarose gel electrophoresis.

Results

Flow cytometry data showed that VAD induced cell cycle arrest at the G0/G1 checkpoint and significantly upregulated caspase-3 in treated cells compared to the control cells. Agarose gel electrophoresis resulted in the formation of DNA ladders in VAD-treated cells. Conclusions: These results suggest that inhibition of cancer cell growth, induction of cell cycle arrest, and apoptosis through caspase-3 activation and nucleosomal DNA fragmentation are involved in the therapeutic mechanisms of VAD as a candidate drug towards the prevention and/or treatment of PCa.

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