Moringa Oleferia Extracts Inhibit Proliferation in Triple-Negative Breast Cancer Cell Lines

摘要

Moringa oleferia is a plant composed of antioxidant properties, polyphenols, and other valuable nutrients and amino acids, namely vitamin c and lysine. Given that the composition of moringa is nutritious and beneficial, the plant has also been utilized for medicinal applications. Moringa has been employed as an antifungal and antibacterial agent and has been shown to treat chronic diseases, including hypertension, diabetes, and certain cancers. Triple-negative breast cancer (TNBC) accounts for 15% of all breast cancers. It is one of the most aggressive types of breast cancer due to the cancerous cells being able to divide quickly and metastasize regularly. TNBC received its name because the cancer cells test negative for the progesterone receptor, estrogen receptor, and the HER2 protein. These three receptors are frequently found in breast cancers and are used as drug therapy targets. However, patients diagnosed with TNBC lack these receptors, limiting treatment options. Due to the limited treatment options provided for TNBC, other alternatives, such as natural products that possess anticancer properties, are being explored.The main objective of this study is to investigate the impact of moringa extracts (M.E.) on breast cancer cell proliferation on cell lines HCC1806, HCC70, and HCC1500. The breast cancer cell lines were treated with M.E. at 24 h and 48 h with varying concentrations of M.E. ranging from100 μg/ml, 50 μg/ml, 25 μg/ml, 12.5 μg/ml, and 2.5 μg/ml. Following treatments with the M.E.,MTT assays were performed to evaluate the effect on cell proliferation. The data demonstrate that M.E. can inhibit cell proliferation of the breast cancer cell lines when exposed to M.E. for 24h and 48 h. In addition, the molecular mechanism of how M.E. suppresses breast cancer cell proliferation was investigated. Caspases 3 and 7 are prominent indicators of apoptosis occurring in the cells. An apotox luminescent assay, which can detect the cleavage of caspase 3 and 7, was performed to assess the M.E. potential to initiate apoptosis in the breast cancer lines. The breast cancer cell lines were treated with M.E. with concentrations of 100 μg/ml, 50 μg/ml, and 2.5μg/ml at 24 h and 48 h. The apotox assay showed that M.E. at concentrations of 100 μg/ml and50 μg/ml have low amounts of caspase 3/7 activity for 24 h and 48 h. Another indicator of apoptosis is PARP cleavage, an essential enzyme responsible for repairing DNA. HCC 1806, HCC70, and HCC1500 were treated with M.E. 48 h before lysis and probed for full length and cleaved PARP. The results showed cleaved PARP could be detected in the 100 μg/ml, 50 μg/ml, and 2.5 μg/ml of M.E. for some cell lines. In addition, M.E. at concentrations of 100 μg/ml and12.5 μg/ml was combined with a known chemotherapy reagent, doxorubicin (1μM). This was to determine whether M.E can increase the efficiency of doxorubicin. It was found that doxorubicin combined with 12.5 μg/ml of M.E. could lower cell proliferation in all three cells compared to a standalone 12.5 μg/ml of M.E. for 48 h. Given these findings, M.E. can decrease breast cancer cell proliferation, making it a potential chemotherapeutic reagent. In addition, further research is needed to explore the molecular mechanism of M.E.'s effects on breast cancer cell proliferation.