Objective To discuss on mechanism of the killing and apoptosis inducing effect induced by total alkaloid in the CSS(Capparis spinosa L.saponin,CSS)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect o...Objective To discuss on mechanism of the killing and apoptosis inducing effect induced by total alkaloid in the CSS(Capparis spinosa L.saponin,CSS)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect of the CSS on human hepatocarcinoma cell Line HepG-2 was observed by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.This test was signed to observe the changes of the cell cycle of HepG-2 cells affected by the CSS by PI single-staining,and to observe if there were typical apoptosis peaks.The apoptosis inducing effect and changing of mitochondria membrane potential of the CSS on the HepG-2 cells were studied by flow cytometry.The effect of intracellular Ca2+ level of CSS on the HepG-2 cells was measured by laser confocal microscope.Results CSS has growth inhibiting on the HepG-2 and seems to be enhanced with the increasing concentration of CSS,and its IC50 value was 46.16 μg·mL-1.The HepG-2 cells are characteristic apoptosis morphologic changed,and the apoptosis percentage is increased to 66.652% in the 50 μg·mL-1 dosage group.The cells cycle has been changed obviously that the progresses of cells cycle of G1 period and G2 period in high dosage group have been blocked,and the cellular proportion in G2 period is decreased by the function of CSS for 24 h.The mitochondria membrane potential of HepG-2 cells induced by CSS is decreased in various degrees.In addition,the intracellular Ca2+ level is increased by the function of CSS in the middle and high dose groups.Conclusions The CSS has obviously killing and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.展开更多
Objective: To study apoptosis induced by radiation in two nasopharyngeal carcinoma (NPC) cell lines, CNE and CNE-2. Methods: Hoechst 33342 staining, immuno-histochemical staining, RT-PCR, DNA dot blotting and Southern...Objective: To study apoptosis induced by radiation in two nasopharyngeal carcinoma (NPC) cell lines, CNE and CNE-2. Methods: Hoechst 33342 staining, immuno-histochemical staining, RT-PCR, DNA dot blotting and Southern blotting were used to identify apoptosis. Results: A single dose of X-irradiation resulted in apoptosis, the apoptotic index (AI) was time- and dose-dependent. Different apoptotic responses existed in the two cell lines. Immunohistochemical staining showed that bcl-2 protein was strongly positive in CNE but negative in CNE-2. However, RT-PCR revealed p53 mRNA in CNE-2 but not in CNE. P53 and bcl-2 genes were both present in the two cell lines as shown by DNA blotting, but the 2.8 kb fragment of the p53 gene was much lower than the 5.6 kb fragment on CNE which was clearly shown in Southern hybridization, suggestive of partial deletion of p53 gene in CNE. Conclusion: Apoptotic response to radiation is different in two NPC cell lines. CNE is more radioresistant than CNE-2. Overexpression of bcl-2 protein and partial deletion of p53 gene may explain their difference in radiosensitivity.展开更多
Objective To study on the mechanism of killing and apoptosis inducing effect of total alkaloid in the CSA(Capparis spinosa L.alkaloid,CSA)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect of the CSA...Objective To study on the mechanism of killing and apoptosis inducing effect of total alkaloid in the CSA(Capparis spinosa L.alkaloid,CSA)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect of the CSA on human hepatocarcinoma cell Line HepG-2 was measured by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.The apoptosis inducing effect and changing of mitochondria membrane potential of the CSA on the HepG-2 cells were measured by flow cytometry.In addition,effect of intracellular Ca2+ level of the CSA on the HepG-2 cells was studied by laser confocal microscope.Results The CSA has obvious cytotoxicity on the HepG-2 and seems to be dose-dependent,and its IC50 value is 162.4 μg·mL-1.The HepG-2 cells have characteristic morphologic changes of apoptosis by the function of CSA,and the apoptosis percentage is higher than the natural one.The progress of cells cycle from S phase to G2 phase has been blocked,and the mitochondria membrane potential is markedly decreased,and the intracellular Ca2+ level is increased by the function of CSA.Conclusions The CSA has obviously killing and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.展开更多
Objective To study on the mechanism of growth inhibiting and apoptosis inducing effect of total alkaloid in the CSEO(Capparis spinosa L.essential oil,CSEO)on human hepatocarcinoma cell Line HepG-2.Methods The growth i...Objective To study on the mechanism of growth inhibiting and apoptosis inducing effect of total alkaloid in the CSEO(Capparis spinosa L.essential oil,CSEO)on human hepatocarcinoma cell Line HepG-2.Methods The growth inhibiting effect of the CSEO on human hepatocarcinoma cell Line HepG-2 was measured by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.The changing of mitochondrion membrane potential induced by CSEO was observed by staining with Rhodamine123.Effect of the CSEO on intracellular Ca2+ level of the HepG-2 cells was measured by laser confocal microscope.Results The CESO has obvious growth inhibiting effect on the HepG-2 and seems to be dose-dependent,and its IC50 is 127.5 μg·mL-1.The characteristic apoptosis morpha of HepG-2 cells has been observed,and the apoptosis percentage increase to 44.447% in the 300 μg·mL-1 dosage group.In addition,the progress of cells cycle of G1 period has been blocked,and the cellular proportion in S and G2 period is decreased in the 75 μg·mL-1 and 150 μg·mL-1 dosage groups by the function of CSEO for 48 h.The mitochondria membrane potential(Δψm)effected by CESO is decreased,while the curve moves toward left.In addition,the intracellular Ca2+ level is increased by the function of CESO in the middle and high dose groups.Conclusions The CESO has obviously growth inhibiting and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.展开更多
AIM:To investigate the change in expression of p53 ,Bcl-2 ,and Bax genes in human colon cancer cells transplanted into nude mice after hyperthermia,chemotherapy,radiotherapy,thermochemotherapy,thermoradiotherapy and t...AIM:To investigate the change in expression of p53 ,Bcl-2 ,and Bax genes in human colon cancer cells transplanted into nude mice after hyperthermia,chemotherapy,radiotherapy,thermochemotherapy,thermoradiotherapy and thermochemoradiotherapy. METHODS:Human colon cancer cell line (HT29) was transplanted into the hind limbs of nude mice. Under laboratory simulated conditions of hyperthermia (43℃,60 min),the actual radiation doses and doses of mitomycin C (MMC) were calculated in reference to the clinical radiotherapy for human rectal cancer and chemotherapy prescription for colon cancer. The mice were divided into 6 groups according to the treatment approaches:hyperthermia,chemotherapy,radiotherapy,thermochemotherapy,thermoradiotherapy,and thermochemoradiotherapy. The mice were sacrificed at different time points and the tumor tissue was taken for further procedures. The morphologic changes in membrane,cytoplasm and nuclei of tumor cells of p53,Bcl-2,and Bax after treatment,were observed by immunohistochemistry staining. RESULTS:All of the six treatment modalities down-regulated the expression of p53,Bcl-2 and up-regulated the expression of Bax at different levels. The combined therapy of hyperthermia,with chemotherapy,and/or irradiation showed a greater effect on down-regulating the expression of p53 (0.208 ± 0.009 vs 0.155 ± 0.0115,P < 0.01) and Bcl-2 (0.086 ± 0.010 vs 0.026 ± 0.0170,P < 0.01) and up-regulating Bax expression (0.091 ± 0.0013 vs 0.207 ± 0.027,P < 0.01) compared with any single therapy.CONCLUSION:Hyperthermia enhances the effect of radio-and chemotherapy on tumors by changing the expression of apoptosis genes,such as p53,Bcl-2 and Bax.展开更多
Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET ...Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET （0, 2, 10, and 50 mM）. The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytornetry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species （ROS） generated by HepG2 cells after treat- ment. Results： MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the produc- tion of ROS in HepG2 cells. Conclusion： MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation.展开更多
Objective To evaluate the effects of arsenic trioxide (As-2O-3) on apoptosis and differentiation of gastric cancer cell lines (GCCL). Methods MKN45 and SGC7901 cells were treated with As-2O-3 at different concentratio...Objective To evaluate the effects of arsenic trioxide (As-2O-3) on apoptosis and differentiation of gastric cancer cell lines (GCCL). Methods MKN45 and SGC7901 cells were treated with As-2O-3 at different concentrations, then the apoptosis rates and cell cycle were determined by flow cytometry assays, the morphologic changes were observed under fluorescence microscopy and electronic microscopy, and the gene expressions were tested with immunohistologic staining. Results Higher apoptosis rates of GCCL were seen in the As-2O-3-treated group at concentrations of 5μmol and 10μmol, as compared with those in the 5-Fu-treated group. Cell-nuclear pyknosis and chromosomal condensation were observed. The As-2O-3 at a concentration of 0.5 μmol could induce the cell cycle changes of GCCL, revealing an increase in the proportion of G1/G0 phase cells and a decrease in the proportion of S phase cells. From the fifth day after treatment of SGC7901 with As-2O-3 at a low concentration, P53 and bcl-XL genes expression rates were reduced, Bax gene expression rate increased, and bcl-2 gene expression showed little change. Conclusion As-2O-3 could induce GCCL apoptosis at a high concentration and differentiation at a low concentration, but it could not completely reverse the malignant biological behaviours of cancer cells.展开更多
Objective To observe the effect of meisoindigo onapoptosis and proliferation of JAK2 /V617F heterozygousmutation cell line-SET2 cell line to further explore therole of JAK-STAT pathway in this effect. Methods Cellapop...Objective To observe the effect of meisoindigo onapoptosis and proliferation of JAK2 /V617F heterozygousmutation cell line-SET2 cell line to further explore therole of JAK-STAT pathway in this effect. Methods Cellapoptosis after treated with different concentration of meisoindigo(0,5,and 10 μmol /L) was evaluated by flowcytometry at different time points (24,48,72 h). Cellproliferation with CCK8 test was evaluated at differenttime points (24,48,72,96 h) after administered withdifferent concentration of meisoindigo (0,5,10,and20 μmol /L). After treatment with different concentrationof meisoindigo (0,5,10,and 20 μmol /L),SET2 cellswere collected after 12 h,and then cultured in incom-plete methylcellulose-based medium for clone formation.JAK-STAT signaling pathway and apoptosis related proteinby Western blot test were evaluated 12 h after administeredwith different concentration of meisoindigo(0,5,10,and 20 μmol /L).展开更多
Objective To investigate arsenic trioxide (As 2O 3)-induced apoptosis and the effects on cell nuclear matrix related protein promyelocytic leukaemia (PML). Methods HepG2 cells were cultured in MEM medium and treat...Objective To investigate arsenic trioxide (As 2O 3)-induced apoptosis and the effects on cell nuclear matrix related protein promyelocytic leukaemia (PML). Methods HepG2 cells were cultured in MEM medium and treated with 0.5, 2, 5 and 10 μmol/L As 2O 3 for either 24 h or 96 h at each concentration. In situ terminal deoxynucleotidyl transferase (TdT) labeling (TUNEL) and DNA ladders were used to detect apoptosis. Confocal microscopy and Western blotting were used to observe the expression of PML. Results The growth rates of HepG2 cells were slower in the As 2O 3 treated than the untreated control group. DNA ladder and TUNEL positive apoptotic cells could be detected in As 2O 3 treated groups. The expression of PML decreased in HepG2 cells with 2 μmol/L As 2O 3 treatment. Confocal images demonstrated that the expression of PML protein in HepG2 cell nuclei decreased after treatment with 2 μmol/L As 2O 3, and micropunctates characteristic of PML protein in HepG2 cell nuclei disappeared after treatment with 5 μmol/L As 2O 3.Conclusions Our results show that arsenic trioxide can significantly inhibit the growth of HepG2 cells in vitro. As 2O 3 induces apoptosis in HepG2 tumor cells in a time and concentration dependent manner. As 2O 3 may degrade the PML protein in HepG2 cell nuclei. The decreased expression of PML in As 2O 3 treated tumor cells is most likely to be caused by apoptosis. Nuclear matrix associated protein PML could be the target of As 2O 3 therapy.展开更多
文摘Objective To discuss on mechanism of the killing and apoptosis inducing effect induced by total alkaloid in the CSS(Capparis spinosa L.saponin,CSS)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect of the CSS on human hepatocarcinoma cell Line HepG-2 was observed by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.This test was signed to observe the changes of the cell cycle of HepG-2 cells affected by the CSS by PI single-staining,and to observe if there were typical apoptosis peaks.The apoptosis inducing effect and changing of mitochondria membrane potential of the CSS on the HepG-2 cells were studied by flow cytometry.The effect of intracellular Ca2+ level of CSS on the HepG-2 cells was measured by laser confocal microscope.Results CSS has growth inhibiting on the HepG-2 and seems to be enhanced with the increasing concentration of CSS,and its IC50 value was 46.16 μg·mL-1.The HepG-2 cells are characteristic apoptosis morphologic changed,and the apoptosis percentage is increased to 66.652% in the 50 μg·mL-1 dosage group.The cells cycle has been changed obviously that the progresses of cells cycle of G1 period and G2 period in high dosage group have been blocked,and the cellular proportion in G2 period is decreased by the function of CSS for 24 h.The mitochondria membrane potential of HepG-2 cells induced by CSS is decreased in various degrees.In addition,the intracellular Ca2+ level is increased by the function of CSS in the middle and high dose groups.Conclusions The CSS has obviously killing and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.
文摘Objective: To study apoptosis induced by radiation in two nasopharyngeal carcinoma (NPC) cell lines, CNE and CNE-2. Methods: Hoechst 33342 staining, immuno-histochemical staining, RT-PCR, DNA dot blotting and Southern blotting were used to identify apoptosis. Results: A single dose of X-irradiation resulted in apoptosis, the apoptotic index (AI) was time- and dose-dependent. Different apoptotic responses existed in the two cell lines. Immunohistochemical staining showed that bcl-2 protein was strongly positive in CNE but negative in CNE-2. However, RT-PCR revealed p53 mRNA in CNE-2 but not in CNE. P53 and bcl-2 genes were both present in the two cell lines as shown by DNA blotting, but the 2.8 kb fragment of the p53 gene was much lower than the 5.6 kb fragment on CNE which was clearly shown in Southern hybridization, suggestive of partial deletion of p53 gene in CNE. Conclusion: Apoptotic response to radiation is different in two NPC cell lines. CNE is more radioresistant than CNE-2. Overexpression of bcl-2 protein and partial deletion of p53 gene may explain their difference in radiosensitivity.
文摘Objective To study on the mechanism of killing and apoptosis inducing effect of total alkaloid in the CSA(Capparis spinosa L.alkaloid,CSA)on human hepatocarcinoma cell Line HepG-2.Methods The killing effect of the CSA on human hepatocarcinoma cell Line HepG-2 was measured by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.The apoptosis inducing effect and changing of mitochondria membrane potential of the CSA on the HepG-2 cells were measured by flow cytometry.In addition,effect of intracellular Ca2+ level of the CSA on the HepG-2 cells was studied by laser confocal microscope.Results The CSA has obvious cytotoxicity on the HepG-2 and seems to be dose-dependent,and its IC50 value is 162.4 μg·mL-1.The HepG-2 cells have characteristic morphologic changes of apoptosis by the function of CSA,and the apoptosis percentage is higher than the natural one.The progress of cells cycle from S phase to G2 phase has been blocked,and the mitochondria membrane potential is markedly decreased,and the intracellular Ca2+ level is increased by the function of CSA.Conclusions The CSA has obviously killing and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.
文摘Objective To study on the mechanism of growth inhibiting and apoptosis inducing effect of total alkaloid in the CSEO(Capparis spinosa L.essential oil,CSEO)on human hepatocarcinoma cell Line HepG-2.Methods The growth inhibiting effect of the CSEO on human hepatocarcinoma cell Line HepG-2 was measured by MTT method.Morphological observation of the HepG-2 cells was completed by fluorescence microscope.The changing of mitochondrion membrane potential induced by CSEO was observed by staining with Rhodamine123.Effect of the CSEO on intracellular Ca2+ level of the HepG-2 cells was measured by laser confocal microscope.Results The CESO has obvious growth inhibiting effect on the HepG-2 and seems to be dose-dependent,and its IC50 is 127.5 μg·mL-1.The characteristic apoptosis morpha of HepG-2 cells has been observed,and the apoptosis percentage increase to 44.447% in the 300 μg·mL-1 dosage group.In addition,the progress of cells cycle of G1 period has been blocked,and the cellular proportion in S and G2 period is decreased in the 75 μg·mL-1 and 150 μg·mL-1 dosage groups by the function of CSEO for 48 h.The mitochondria membrane potential(Δψm)effected by CESO is decreased,while the curve moves toward left.In addition,the intracellular Ca2+ level is increased by the function of CESO in the middle and high dose groups.Conclusions The CESO has obviously growth inhibiting and apoptosis inducing effect on human hepatocarcinoma cell Line HepG-2 by the mechanism of decreasing the mitochondria membrane potential and increasing the intracellular Ca2+ level.
基金Supported by the Clinical Research Foundation of Tianjin Medical University, No. 2002KY18
文摘AIM:To investigate the change in expression of p53 ,Bcl-2 ,and Bax genes in human colon cancer cells transplanted into nude mice after hyperthermia,chemotherapy,radiotherapy,thermochemotherapy,thermoradiotherapy and thermochemoradiotherapy. METHODS:Human colon cancer cell line (HT29) was transplanted into the hind limbs of nude mice. Under laboratory simulated conditions of hyperthermia (43℃,60 min),the actual radiation doses and doses of mitomycin C (MMC) were calculated in reference to the clinical radiotherapy for human rectal cancer and chemotherapy prescription for colon cancer. The mice were divided into 6 groups according to the treatment approaches:hyperthermia,chemotherapy,radiotherapy,thermochemotherapy,thermoradiotherapy,and thermochemoradiotherapy. The mice were sacrificed at different time points and the tumor tissue was taken for further procedures. The morphologic changes in membrane,cytoplasm and nuclei of tumor cells of p53,Bcl-2,and Bax after treatment,were observed by immunohistochemistry staining. RESULTS:All of the six treatment modalities down-regulated the expression of p53,Bcl-2 and up-regulated the expression of Bax at different levels. The combined therapy of hyperthermia,with chemotherapy,and/or irradiation showed a greater effect on down-regulating the expression of p53 (0.208 ± 0.009 vs 0.155 ± 0.0115,P < 0.01) and Bcl-2 (0.086 ± 0.010 vs 0.026 ± 0.0170,P < 0.01) and up-regulating Bax expression (0.091 ± 0.0013 vs 0.207 ± 0.027,P < 0.01) compared with any single therapy.CONCLUSION:Hyperthermia enhances the effect of radio-and chemotherapy on tumors by changing the expression of apoptosis genes,such as p53,Bcl-2 and Bax.
文摘Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET （0, 2, 10, and 50 mM）. The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytornetry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species （ROS） generated by HepG2 cells after treat- ment. Results： MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the produc- tion of ROS in HepG2 cells. Conclusion： MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation.
文摘Objective To evaluate the effects of arsenic trioxide (As-2O-3) on apoptosis and differentiation of gastric cancer cell lines (GCCL). Methods MKN45 and SGC7901 cells were treated with As-2O-3 at different concentrations, then the apoptosis rates and cell cycle were determined by flow cytometry assays, the morphologic changes were observed under fluorescence microscopy and electronic microscopy, and the gene expressions were tested with immunohistologic staining. Results Higher apoptosis rates of GCCL were seen in the As-2O-3-treated group at concentrations of 5μmol and 10μmol, as compared with those in the 5-Fu-treated group. Cell-nuclear pyknosis and chromosomal condensation were observed. The As-2O-3 at a concentration of 0.5 μmol could induce the cell cycle changes of GCCL, revealing an increase in the proportion of G1/G0 phase cells and a decrease in the proportion of S phase cells. From the fifth day after treatment of SGC7901 with As-2O-3 at a low concentration, P53 and bcl-XL genes expression rates were reduced, Bax gene expression rate increased, and bcl-2 gene expression showed little change. Conclusion As-2O-3 could induce GCCL apoptosis at a high concentration and differentiation at a low concentration, but it could not completely reverse the malignant biological behaviours of cancer cells.
文摘Objective To observe the effect of meisoindigo onapoptosis and proliferation of JAK2 /V617F heterozygousmutation cell line-SET2 cell line to further explore therole of JAK-STAT pathway in this effect. Methods Cellapoptosis after treated with different concentration of meisoindigo(0,5,and 10 μmol /L) was evaluated by flowcytometry at different time points (24,48,72 h). Cellproliferation with CCK8 test was evaluated at differenttime points (24,48,72,96 h) after administered withdifferent concentration of meisoindigo (0,5,10,and20 μmol /L). After treatment with different concentrationof meisoindigo (0,5,10,and 20 μmol /L),SET2 cellswere collected after 12 h,and then cultured in incom-plete methylcellulose-based medium for clone formation.JAK-STAT signaling pathway and apoptosis related proteinby Western blot test were evaluated 12 h after administeredwith different concentration of meisoindigo(0,5,10,and 20 μmol /L).
文摘Objective To investigate arsenic trioxide (As 2O 3)-induced apoptosis and the effects on cell nuclear matrix related protein promyelocytic leukaemia (PML). Methods HepG2 cells were cultured in MEM medium and treated with 0.5, 2, 5 and 10 μmol/L As 2O 3 for either 24 h or 96 h at each concentration. In situ terminal deoxynucleotidyl transferase (TdT) labeling (TUNEL) and DNA ladders were used to detect apoptosis. Confocal microscopy and Western blotting were used to observe the expression of PML. Results The growth rates of HepG2 cells were slower in the As 2O 3 treated than the untreated control group. DNA ladder and TUNEL positive apoptotic cells could be detected in As 2O 3 treated groups. The expression of PML decreased in HepG2 cells with 2 μmol/L As 2O 3 treatment. Confocal images demonstrated that the expression of PML protein in HepG2 cell nuclei decreased after treatment with 2 μmol/L As 2O 3, and micropunctates characteristic of PML protein in HepG2 cell nuclei disappeared after treatment with 5 μmol/L As 2O 3.Conclusions Our results show that arsenic trioxide can significantly inhibit the growth of HepG2 cells in vitro. As 2O 3 induces apoptosis in HepG2 tumor cells in a time and concentration dependent manner. As 2O 3 may degrade the PML protein in HepG2 cell nuclei. The decreased expression of PML in As 2O 3 treated tumor cells is most likely to be caused by apoptosis. Nuclear matrix associated protein PML could be the target of As 2O 3 therapy.
