Authors

MIAO YU*, **, YUBIN JI*, **, KAILIN CHANG*, **, SHIYONG GAO*, **, CHENFENG JI*, **, GOUSONG XIN*, **

Departments

*Research Center on Life Sciences and Environmental Sciences, Harbin University of Commerce, Harbin,150076, China - **Engineering Research Center of Natural Anticancer Drugs, Ministry of Education, Harbin,150076, China

Abstract

Introduction: Lycorine is a natural alkaloid, existing largly in the Amaryllidaceae plant family. It has a wide range of pharmacological activity. Recent studies have found that lycorine has significant effect on the hematological malignancies. However, the effect of lycorine on the Human breast cancer MCF-7 cells (MCF-7) are not clear. In this context, we studied that lycorine induced the apoptosis of MCF-7 cells, and explored the possible mechanism of it.

Materials and methods: The MCF-7 cells were treated with different concentrations of lycorine for 72h. The inhibition rate of the MCF-7 cells was detected with Brominated tetrazolium (MTT) assay, cell morphology was observed using an inverted microscope, the change of cell intracellular calcium and membrane potential was detected with confocal laser scanning microscope.

Results: MTT assay showed that lycorine could inhibit the MCF-7 growth in dose-dependent manner after 72h. The MCF-7 cells were rupture and dead under inverted microscope. Calcium concentration in MCF-7 cells significantly increased and membrane potential were decreased in dose-dependent manner.Disscussion: These results showed that lycorine could inhibit the MCF-7 cells growth and induce it apoptosis, the mechanism might involve an initiation of apoptosis signals in the mitochondrial pathway. This research first discovered

Disscussion: These results showed that lycorine could inhibit the MCF-7 cells growth and induce it apoptosis, the mechanism might involve an initiation of apoptosis signals in the mitochondrial pathway. This research first discovered anti-tumor mechanism of lycorine on MCF-7 cells.

Keywords

Lycorine, Human Breast Cancer, Apoptosis, mitochondrial pathway.

DOI:

10.19193/0393-6384_2016_6_161