Emodin Induces Death in Human Cervical Cancer Cells Through Mitotic Catastrophe

Abstract

Background: Anthraquinones, including emodin, are compounds with numerous pharmacological properties, including anticancer properties. The aim of this study experiment was to examine the effect of emodin, a natural compound present in the roots and rhizomes of Rheum palmatum, on the induction of mitotic catastrophe in cervical cancer cells. Material and Methods: HeLa celIs were treated with different emodin concentrations for 48 h, and cell growth was measured with 3-(4-,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolyl. The cell-cycle distribution and the level of apoptosis were determined by means of flow cytometry, using annexin V-fluorescein isothiocyanate staining and propidium iodide. Morphological changes in the mitotic apparatus were evaluated using optical and confocal microscopy techniques. Results: Emodin induced an increase in the number of polymorphonuclear cells, giant cells, cells with micronuclei, cells with abnormal mitosis and damaged spindle. The reorganization of F-actin depended on the concentration of emodin. With the increase in emodin concentration, inhibition of mitotic activity was demonstrated, which was manifested by a decrease in the mitotic index, mainly in metaphase of the mitotic process and an increase in the number of cells inhibited in the G 2 /M phase. At the same time, an increase in the number of apoptotic cells was found. Conclusion: Emodin leads to death of cervical cancer cells by induction of a mitotic catastrophe.

Progress on the Study of the Anti-Tumor Effect of Emodin

“…The inhibitory effect of emodin on cell division was highest at 100 μM. Besides, emodin can also damage the cytoskeleton [41].…”

“…Besides, emodin can also increase the membrane permeability of lysosomes, decrease the activities of cathepsin D and L in lysosomes, and increase the activity of proteolytic enzymes [21]. There are also research findings that emodin can make cervical cancer cell cycle disorder and apoptosis increase [41]. This is mainly due to the inhibition of mitotic activity by emodin.…”

Is Emodin with Anticancer Effects Completely Innocent? Two Sides of the Coin

“…In their later study, Trybus et al again discussed the apoptotic mechanism of emodin in HeLa cells in the concentration range of 1–100 μM. According to the results, it caused the highest inhibition of cell division at 100 μM, caused G2/M phase cell cycle arrest, enhanced the number of cells undergoing mitotic catastrophe, and increased changes in the cytoskeleton [ 152 ]. In vitro biochemical effects of emodin in cervical cancer cell lines are summarized in Table 7 .…”

Antitumor Effects of Self-Assembling Peptide-Emodin in situ Hydrogels in vitro and in vivo

“…It has been cumulatively documented that EM causes cell growth inhibition via an apoptotic mechanism. 52,53 In the current work, Hepa1-6 cells were employed to investigate the apoptotic process caused by free EM and RADA16-I-EM hydrogels. As shown in Figure 5, untreated Hepa1-6 cells showed little apoptosis and necrosis (early apoptosis: ~2.4%, late apoptosis: ~2.9%, and necrosis: ~1.1%); when the final concentration of EM reached 200 μM, free EM led to increases in both cellular apoptosis and necrosis: ~3.3% early apoptosis, ~18.2% late apoptosis, and ~10.2% necrosis.…”