AI Article Synopsis
- Condurango extract (CE) is traditionally used in alternative medicine, particularly for treating syphilis, and has shown potential to reduce tumor volume, though its specific mechanisms are not yet fully understood.
- Researchers examined CE's anticancer effects on cervical cancer (HeLa) and other cancer cell lines using various techniques, which indicated CE's cytotoxicity is linked to the generation of reactive oxygen species (ROS) and is influenced by DNA damage.
- The study found that CE increased levels of tumor necrosis factor alpha (TNF-α) and activated pathways leading to apoptosis, while decreasing protective signals such as NF-κB, suggesting specific molecular pathways for its anticancer effects.
Article Abstract
Objectives: Condurango (Gonolobus condurango) extract is used by complementary and alternative medicine (CAM) practitioners as a traditional medicine, including homeopathy, mainly for the treatment of syphilis. Condurango bark extract is also known to reduce tumor volume, but the underlying molecular mechanisms still remain unclear.
Methods: Using a cervical cancer cell line (HeLa) as our model, the molecular events behind condurango extract's (CE's) anticancer effect were investigated by using flow cytometry, immunoblotting and reverse transcriptase-polymerase chain reaction (RT-PCR). Other included cell types were prostate cancer cells (PC3), transformed liver cells (WRL-68), and peripheral blood mononuclear cells (PBMCs).
Results: Condurango extract (CE) was found to be cytotoxic against target cells, and this was significantly deactivated in the presence of N-acetyl cysteine (NAC), a scavenger of reactive oxygen species (ROS), suggesting that its action could be mediated through ROS generation. CE caused an increase in the HeLa cell population containing deoxyribonucleic acid (DNA) damage at the G zero/Growth 1 (G0/G1) stage. Further, CE increased the tumor necrosis factor alpha (TNF-α) and the fas receptor (FasR) levels both at the ribonucleic acid (RNA) and the protein levels, indicating that CE might have a cytotoxic mechanism of action. CE also triggered a sharp decrease in the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB ) both at the RNA and the protein levels, a possible route to attenuation of B-cell lymphoma 2 (Bcl-2), and caused an opening of the mitochondrial membrane's permeability transition (MPT) pores, thus enhancing caspase activities.
Conclusion: Overall, our results suggest possible pathways for CE mediated cytotoxicity in model cancer cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573805 | PMC |
| http://dx.doi.org/10.3831/KPI.2015.18.022 | DOI Listing |
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