Abstract
BackgroundKalanchoe tubiflora (KT) is a succulent plant native to Madagascar, and is commonly used as a medicinal agent in Southern Brazil. The underlying mechanisms of tumor suppression are largely unexplored.MethodsCell viability and wound-healing were analyzed by MTT assay and scratch assay respectively. Cell cycle profiles were analyzed by FACS. Mitotic defects were analyzed by indirect immunofluoresence images.ResultsAn n-Butanol-soluble fraction of KT (KT-NB) was able to inhibit cell proliferation. After a 48 h treatment with 6.75 μg/ml of KT, the cell viability was less than 50% of controls, and was further reduced to less than 10% at higher concentrations. KT-NB also induced an accumulation of cells in the G2/M phase of the cell cycle as well as an increased level of cells in the subG1 phase. Instead of disrupting the microtubule network of interphase cells, KT-NB reduced cell viability by inducing multipolar spindles and defects in chromosome alignment. KT-NB inhibits cell proliferation and reduces cell viability by two mechanisms that are exclusively involved with cell division: first by inducing multipolarity; second by disrupting chromosome alignment during metaphase.ConclusionKT-NB reduced cell viability by exclusively affecting formation of the proper structure of the mitotic apparatus. This is the main idea of the new generation of anti-mitotic agents. All together, KT-NB has sufficient potential to warrant further investigation as a potential new anticancer agent candidate.
Highlights
Kalanchoe tubiflora (KT) is a succulent plant native to Madagascar, and is commonly used as a medicinal agent in Southern Brazil
KT-NB decreases cell viability We treated HeLa cells with different doses of KT-NB to analyze its effect of cell proliferation
Cells were exposed to three different concentrations of KT-NB and DMSO, which was used as a control
Summary
Kalanchoe tubiflora (KT) is a succulent plant native to Madagascar, and is commonly used as a medicinal agent in Southern Brazil. Far two major pathways have been identified in mitotic spindle assembly. The mitotic centrosomes function as microtubuleorganizing centers (MTOCs) [1], directing spindle assembly from spindle poles through the regulation of nucleating microtubules [2]. The second pathway is dependent on a RanGTP gradient mediated by Aurora A, which regulates spindle assembly [3,4]. The chromosomal passenger complex (CPC) generates spindle assembly in the absence of a RanGTP gradient [5,6]. Disruption of these pathways and disruption of the mitotic spindle will
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