Evaluation of Cytotoxicity and Anti-tumor Effect of Salvia sahandica’s Fragments on MCF-7 Breast Cancer Cell-Lines
Abstract
Introduction: Cancer causes significant morbidity and mortality and is a major public health problem worldwide. Plant-derived compounds have been an important source of several clinically useful anti-cancer agents. S. sahehandica have been used in Azarbaijan folk medicine for treatment of various diseases.
Aim: In the current study we aimed to assess cytotoxic and possible anti-cancer effects of this plant on MCF-7 breast cancer cell line.
Materials and Methods: The cells were exposed to A-F compounds extracted from petrolatum ether extract of S.sahehandica at different concentrations and time durations. Furthermore, apoptosis detection assays were done for distinguishing apoptosis from necrosis. Expression of apoptosis related genes was studied using reverse transcriptase-QPCR.
Results: Our results showed that compounds A, B and C greatly inhibited MCF-7 cell proliferation. Upon treatment with extracts, a clear difference was observed in cellular morphology; the cells acquired more attenuated architecture. Although cytotoxic effect of A was higher, results of apoptosis detection assays demonstrated that compound C acts as an apoptosis activator, where as compounds A and B act as necrosis activator. Furthermore, qPCR showed that activation of the apoptosis is mediated through PI3K/AKT pathway.
Discussion: Based on the results of cellular/molecular experiment we demonstrated that lipophilic extracts of S.sahehandica had in vitro cytotoxic activity and inhibitory effect on the growth of human breast cancer cell line MCF-7. As evidenced from these preliminary results, this medicinal plant may be considered as attractive alternatives to serve as lead compounds in drug development for human breast cancer as an adjuvant therapy.
Conclusion: Collectively, the results suggest that the S.sahehandica root extract has cytotoxic effects on human breast cancer cells by activation of the apoptosis PI3K/AKT pathway.