Inhibition and related mechanisms of different selenium compounds on canine breast cancer cells CTM1211
Liu Yu-zh
Abstract
Liu Yu-zh
Abstract
To evaluate the effect of different doses,forms and compatibility of selenium on canine breast cancer cells CTM1211 and to explore the related mechanisms,CTM1211 cells were intervened by different doses of CTX(cyclophosphamide:1,2,4 mg/mL),SSE(selenite:10,20,40μmol/L),MSA(methylseleninic acid:10,20,40μmol/L),MSC(selenocysteine:200,400,800μmol/L),CTX+SSE(0.5mg/mL+5μmol/L,1 mg/mL+10μmol/L,2 mg/mL+20μmol/L),CTX+ MSA(0.5 mg/mL+5μmol/L,1mg/mL+10μmol/L,2mg/mL+20μmol/L)and CTX+MSC(0.5mg/mL+100μmol/L,1mg/mL+200μmol/L,2mg/mL+400μmol/L)for 24 h,48hand 72 h,and the cell viability of each group was determined by MTT.While simplified cells were intervened by CTX(2 mg/mL),SSE(40μmol/L),MSA(20μmol/L),MSC(400μmol/L)and CTX+MSA(2mg/mL+20μmol/L)for 48 hand the cell apoptosis rate was measured by flow cytometry,the protein and mRNA expression of VEGF-a(vascular endothelial growth factor a),PTEN(phosphatase and tensin homolog),Ang-2(angiopoietin-2)and HIF-1a(hypoxia inducible factor 1a)were measured by immunohistochemistry and RT-qPCR,respectively.The cell viability of each group at 48h/72 hwas significantly lower(P0.01 or P0.05),while the apoptosis ratewas significantly higher at each time point(P0.01)than that of the control group,and the effect of group CTX + MSA was the most significant.Generally,the expression of VEGF-a,Ang-2and HIF-1aprotein and mRNA were significantly low,while that of PTEN were significantly up regulated.In conclusion,selenium,especially MSA,could significantly inhibit breast cancer cell CTM1211,which is partly due to the induction of apoptosis and regulation of tumor angiogenesis-related factors VEGF-a,PTEN,Ang-2and HIF-1aby selenium.
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To evaluate the effect of different doses,forms and compatibility of selenium on canine breast cancer cells CTM1211 and to explore the related mechanisms,CTM1211 cells were intervened by different doses of CTX(cyclophosphamide:1,2,4 mg/mL),SSE(selenite:10,20,40μmol/L),MSA(methylseleninic acid:10,20,40μmol/L),MSC(selenocysteine:200,400,800μmol/L),CTX+SSE(0.5mg/mL+5μmol/L,1 mg/mL+10μmol/L,2 mg/mL+20μmol/L),CTX+ MSA(0.5 mg/mL+5μmol/L,1mg/mL+10μmol/L,2mg/mL+20μmol/L)and CTX+MSC(0.5mg/mL+100μmol/L,1mg/mL+200μmol/L,2mg/mL+400μmol/L)for 24 h,48hand 72 h,and the cell viability of each group was determined by MTT.While simplified cells were intervened by CTX(2 mg/mL),SSE(40μmol/L),MSA(20μmol/L),MSC(400μmol/L)and CTX+MSA(2mg/mL+20μmol/L)for 48 hand the cell apoptosis rate was measured by flow cytometry,the protein and mRNA expression of VEGF-a(vascular endothelial growth factor a),PTEN(phosphatase and tensin homolog),Ang-2(angiopoietin-2)and HIF-1a(hypoxia inducible factor 1a)were measured by immunohistochemistry and RT-qPCR,respectively.The cell viability of each group at 48h/72 hwas significantly lower(P0.01 or P0.05),while the apoptosis ratewas significantly higher at each time point(P0.01)than that of the control group,and the effect of group CTX + MSA was the most significant.Generally,the expression of VEGF-a,Ang-2and HIF-1aprotein and mRNA were significantly low,while that of PTEN were significantly up regulated.In conclusion,selenium,especially MSA,could significantly inhibit breast cancer cell CTM1211,which is partly due to the induction of apoptosis and regulation of tumor angiogenesis-related factors VEGF-a,PTEN,Ang-2and HIF-1aby selenium.
Key concepts: Apoptosis, Mole, Molecular biology, Chemistry, Viability assay, Selenium, Tensin, Vascular endothelial growth factor