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The antitumor effects of selenium compound Na5SeV5O18.3H20 in K562 cell
1School of Life Sciences, Lanzhou University, Lanzhou 730000, P R China.
Abstract:
With an approach to study the anti-tumor effects and mechanism of selenium compound, we investigated the anti-tumor activity and mechanism of Na5SeV5O18.H20 (NaSeVO) in K562 cells. The results showed that 0.625-20 mg/L NaSeVO could significantly inhibit the proliferation of K562 cells in vitro in a time- and concentration-dependent manner as determined by microculture tetrazolium (MTT) assay, the IC50 values were 14.41 (4.45-46.60) and 3.45 (2.29-5.22) mg/L after 48 h and 72 h treatment with NaSeVO respectively. In vivo experiments demonstrated that i.p. administration of 5, 10 mg/kg NaSeVO exhibited an significant inhibitory effect on the growth of transplantation tumor sarcoma 180 (S180) and hepatoma 22 (H22) in mice, with inhibition rate 26.8% and 58.4% on S180 and 31.3% and 47.4% on H22, respectively. Cell cycle studies indicated that the proportion of G0/G1 phase was increased at 2.5 mg/ L while decreased at 10 mg/L after treatment for 24, 48 h. Whereas S phase was decreased at 2.5-5 mg/L and markedly increased at 10 mg/L after treatment for 48 h. After treatment for 24 h, 10 mg/L NaSeVO also markedly increased S and G2/M phases. Take together, the result clearly showed that NaSeVO markedly increased S and G2/M phases at 10 mg/L. The study of immunocytochemistry showed that the expression bcl-2 is significantly inhibited by 10 mg/L NaSeVO, and bax increased. Morphology observation also revealed typical apoptotic features. NaSeVO also significantly caused the accumulation of Ca2+ and Mg2+, reactive oxygen species (ROS) and the reduction of pH value and mitochondrial membrane potential in K562 cells as compared with control by confocal laser scanning microscope. These results suggest that NaSeVO has anti-tumor effects and its mechanism is attributed partially to apoptosis induced by the elevation of intracellular Ca2+, Mg2+ and ROS concentration, and a reduction of pH value and mitochondria membrane potential (MMP).
Insights
Selenium compound Na5SeV5O18.H20 (NaSeVO) shows significant anti-tumor effects against K562 cells and in vivo tumor models. Its mechanism involves inducing apoptosis through altered ion levels, reactive oxygen species, and mitochondrial function.
Area of Science:
- Oncology
- Biochemistry
- Pharmacology
Background:
- Selenium compounds are explored for their anti-tumor potential.
- Understanding the specific mechanisms of novel selenium compounds is crucial for therapeutic development.
Purpose of the Study:
- To investigate the anti-tumor activity and elucidate the mechanism of action of Na5SeV5O18.H20 (NaSeVO).
- To evaluate the efficacy of NaSeVO in vitro against K562 cells and in vivo against sarcoma 180 and hepatoma 22 tumor models.
Main Methods:
- In vitro proliferation inhibition assessed by MTT assay.
- In vivo anti-tumor efficacy evaluated in mouse models (S180 and H22).
- Cell cycle analysis, immunocytochemistry, and confocal laser scanning microscopy were used to study apoptosis and related cellular changes.
Main Results:
- NaSeVO significantly inhibited K562 cell proliferation in a dose- and time-dependent manner (IC50 values provided).
- In vivo studies showed significant tumor growth inhibition for both S180 and H22 models.
- NaSeVO induced apoptosis by altering cell cycle progression (S and G2/M phases), downregulating bcl-2, upregulating bax, and affecting intracellular Ca2+, Mg2+, ROS, pH, and mitochondrial membrane potential.
Conclusions:
- Na5SeV5O18.H20 (NaSeVO) demonstrates potent anti-tumor effects in both in vitro and in vivo models.
- The anti-tumor mechanism of NaSeVO is partially attributed to the induction of apoptosis via modulation of key cellular signaling pathways and organelle functions.
