Abstract 2251: Induction of apoptosis in breast cancer cells using Kedrostis foetidissima.

Abstract

Abstract Kedrostis foetidissima has been used by tribes throught Africa to treat various human livestock ailments. K. foetidissima, has been shown to inhibit the growth of breast cancer cell lines in vitro by induction of apoptosis in previous studies of our group1. With current chemotherapy and radiotherapy continuing to show unwanted side effects the only hope to a better safer medicinal target would include that uses medical plants that induces apoptosis with or without inducing p53 gene2,3. However, the mechanisms of action are not completely understood. In this study we are looking at the role and expressional levels of RBBp6 in breast cancer following treatment with the plant extract. In trying to achieve our objective both human breast cancer tissue and MCF7 cell lines were used to first establish the pattern of expression and then cell lines were treated with medicinal plant to evaluate the expressional patterns using both the immunohistochemistry, RTPCR and Flow cytometer. We observed that protein as well as mRNA level of RBBP6 was inhibited by K. foetidissima in a dose-dependent manner (Fig. 1). However, in both untreated and human breast cancer tissues RBBp6 was found to be highly expressed around cells undergoing cell division. In recent studies, an apoptosis-related gene expression profiling analysis provided a clue that both p53 and bax gene were slightly upregulated at least 2 to 3 fold in response to K. foetidissima treatment in MCF7 cell2. On the other had we have reported in the past that RBBp6 acted as inhibitor of p53 gene. The findings in this study suggest that downregulation of RBBp6 may through small molecules might be a potential therapy in cancer. Citation Format: Lesetja Raymond Motadi. Induction of apoptosis in breast cancer cells using Kedrostis foetidissima. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2251. doi:10.1158/1538-7445.AM2013-2251 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.