DiagnosticvalueofMSCTcombinedwithultrasonographyinpatientswithacuteappendicitis / 实用放射学杂志

Objective ToexploretheclinicalvalueofMSCTcombinedwithultrasonographyinthediagnosisofacuteappendicitis. Methods 238patientswithsuspiciousappendicitisunderwentMSCTandultrasonographybeforesurgery.Allpatientsweredivided intoappendicitisgroupandnormalappendixgroupaccordingtoCTappearances.TheefficacyofMSCTcombinedwithultrasoundin diagnosingappendicitiswasanalyzedbycomparisonofsurgicalpathologicalfindings.Results Therewere220casesinappendicitis group,whichhad165casesofappendicitisconfirmedbypathology,and55casesofnormalappendix.Therewere18casesinnormal group,2caseswereconfirmedappendicitisbypathology,and16caseswerenormalappendix.Theoveralldiagnosticperformancesof theCTscanwere98.8%ofsensitivity,22.5%ofspecificity,82.5%ofpositivepredictivevalue,88.9%ofnegativepredictivevalue, and76.1%ofaccuracy.TheperformancesofMSCTcombinedwithultrasonographywere90.4%ofsensitivity,93.0%ofspecificity, 96.8%ofpositivepredictivevalue,80.5%ofnegativepredictivevalue,and91.2%ofaccuracy.Thedifferencewasstatisticallysignificant indiagnosisperformancesbeforeandafterMSCTcombinedwithultrasonography (P＜0.001).Conclusion MSCTcombinedwith ultrasonographyexaminationcouldimprovethediagnosticaccuracyofappendicitis,andmayreducethenegativerateofappendectomy.

Physical and chemical properties of acetylated low molecular weight heparin and its antineoplastic effect in vitro / 中国药理学通报

Aims To synthesize acetylated low molecu-lar weight heparin( ALMWH) and to detect its physico-chemical properties and antineoplastic activity. Meth-ods LMWH was prepared by degradation of UFH with sodium periodate oxidation and sodium borohydride re-duction, then the LMWH was acetylated by acetic an-hydride where N, N′, -dicyclohexylcarbodiimide ( DCC ) and 4-dimethylaminopyridine ( DMAP ) were used as catalysts. X-ray diffraction(XRD)and Differ-ential Scanning Calorimetry ( DSC ) of ALMWH were obtained. The antiproliferative activity and anti-inva-sive activity were determined on MDA-MB-231 and MCE-7 human breast cancer cells. Results XRD a-nalysis showed that the LMWH degraded from UFH and ALMWH synthesized by acetylation of LMWH be-longed to amorphous structure, however, their DSC curves were significantly different. Compared with LM-WH, ALMWH had more powerful capacity for binding water and lowering anticoagulant activity, more signifi-cantly ALMWH exhibited stranger anti-proliferative and anti-invasive activity than LMWH, especially when it was used in low concentrations. Conclusion The syn-thesized ALMWH possesses a low anticoagulant activi-ty, certain anti-proliferative, anti-invasive and anti-metastatic activity. This study provides a basic method for screening of antineoplastic drug with low toxicity.

Effect of low-molecular-weight heparin combined with doxorubicin on hepatocellular cancer cell migration in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the anti-cancer effect of low-molecular-weight heparin (LMWH) combined with doxorubicin and explore the mechanism.</p><p><b>METHODS</b>Hepatocellular cancer HepG2 cells exposed to LMWH, doxorubicin, or both were evaluated for cell viability with MTT assay and for changes in their migration ability using wound healing assay and Transwell migration assay. The changes in cellular expressions of matrix metalloproteinase-9 (MMP-9) and MMP-2 mRNA and proteins were analyzed with quantitative real-time PCR (qRT-PCR) and Western blotting, and ELISA was used to determine heparanase (HPA) concentration in the cell culture medium.</p><p><b>RESULTS</b>HepG2 cells exhibited suppressed proliferation in response to LMWH and doxorubicin treatments. The combined treatment caused a significantly higher inhibition rate of cell migration than LMWH and doxorubicin alone. LMWH enhanced doxorubicin-induced down-regulation of MMP-9, MMP-2 and HPA in the cells.</p><p><b>CONCLUSIONS</b>LMWH can enhance the inhibitory effect of doxorubicin on the migration of HepG2 cells, the mechanism of which may involve the down-regulation of MMP-9, MMP-2 and HPA expressions.</p>

2-Deoxy-D-glucose combined with Taxol inhibits VEGF expression and induces apoptosis in orthotopically transplanted breast cancer in C3H mice / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the antineoplastic effects of 2-Deoxy-D-glucose (2-DG) combined with Taxol on orthotopically transplanted breast cancer in C3H mice and explore the mechanism.</p><p><b>METHODS</b>C3H mice bearing orthotopically transplanted breast cancer xenograft were randomly divided into 4 groups, namely the control group, 2-DG group, Taxol group, and 2-DG+Taxol group. The corresponding drugs were administered intraperitoneally every 3 days for 18 consecutive days, and the tumor volume was measured every 3 days to draw the tumor growth curve. The mice were then sacrificed to measure the tumor weight on day 19 and examine tumor cell apoptosis with TUNEL assay and VEGF expression using immunohistochemistry.</p><p><b>RESULTS</b>2-DG combined with Taxol obviously suppressed the tumor growth with a tumor inhibition rate of 66.06% as compared to the rate of 36.97% in Taxol group. The combined treatment also caused more obvious cell apoptosis and significantly reduced VEGF expression in the tumor cells as compared with the other groups.</p><p><b>CONCLUSION</b>2-DG can enhance the inhibitory effect of Taxol on orthotopically transplanted breast cancer xenograft in C3H mice probably by inducing tumor cell apoptosis and lowering VEGF expressions.</p>

Effects of metformin on human oral cancer KB cell proliferation and apoptosis in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of metformin on the proliferation and apoptosis of human oral cancer cell line KB in vitro.</p><p><b>METHODS</b>Human oral cancer cell line KB was exposed to different doses of metformin (0, 1.25, 2.5, 5, 10, and 20 mmol/L), and the changes in cell viability were detected using MTT assay. Colony formation of the cells was observed following an 8-day metformin exposure. The changes in mitochondrial membrane potential were measured by JC-1 assay, and PI staining was used to observe the cell apoptosis. Western blotting was employed to detect the changes in the protein expressions of GRP78 and activated caspase-3.</p><p><b>RESULTS</b>Metformin exposure caused time- and dose-dependent suppression of KB cell proliferation, and exposure to 5 mmol/L metformin for 24, 48 and 72 h resulted in cell survival rates of 68.0%, 36.9%, and 14.5%, respectively. Metformin significantly inhibited KB cell colony formation. Exposure of the cells to increased concentrations of metformin gradually increased the apoptotic rate and decreased mitochondrial membrane potential. Metformin caused an initial up-regulation followed by a down-regulation of GRP78 expression in KB cells and increased the expression of activated caspase-3.</p><p><b>CONCLUSION</b>Metformin can inhibit the proliferation and induce apoptosis of KB cells, the mechanism of which may involve the activation of the mitochondrial apoptotic pathway and endoplasmic reticulum stress.</p>

3-bromopyruvate enhances cisplatin sensitivity of hepatocellular carcinoma cells in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of 3-bromopyruvate (3-BP) in sensitizing hepatocellular carcinoma cells to cisplatin-induced apoptosis and its possible mechanism.</p><p><b>METHODS</b>The growth inhibition of HepG2 and SMMC7721 cells following exposures to different concentrations of 3-BP and cisplatin was measured by MTT assay. The apoptosis of cells treated with 100 µmol/L 3-BP with or without 8 µmol/L cisplatin was assessed using flow cytometry with PI staining, and the activity of caspase-3 and intracellular ATP level were detected using commercial detection kits; the expression of XIAP and PARP was analyzed using Western blotting.</p><p><b>RESULTS</b>3-BP produced obvious inhibitory effects on HepG2 and SMMC7721 cells at the concentrations of 50-400 µmol/L with IC50 values of 238.9∓13.9 µmol/L and 278.7∓11.7 µmol/L for a 48-h treatment, respectively. Cisplatin also inhibited the growth of HepG2 and SMMC7721 cells at the concentrations of 2-32 µmol/L, with IC50 values of 16.4∓0.9 µmol/L and 20.9∓1.8 µmol/L after a 48-h treatment, respectively. Treatment with 100 µmol/L 3-BP combined with 8 µmol/L cisplatin for 48 h resulted in a growth inhibition rate of (60.6∓2.2)% in HepG2 cells and (56.8∓2.3)% in SMMC7721 cells, which were significantly higher than those in cells treated with 3-BP or cisplatin alone. The combined treatment for 48 h induced an apoptotic rate of (51.1∓4.3)% in HepG2 cells and (46.5∓3.9)% in SMMC7721 cells, which were also markedly higher than those in cells with 3-BP or cisplatin treatment alone.</p><p><b>CONCLUSION</b>3-BP can sensitize HepG2 and SMMC7721 cells to cisplatin-induced apoptosis possibly by causing intracellular ATP deficiency, down-regulating XIAP, and increasing caspase-3 activity.</p>

Effect of 3-bromopyruvate on mitochondrial membrane potential and apoptosis of human breast carcinoma SK-BR-3 cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of glycolysis inhibitor 3-bromopyruvate (3-BrPA) in inducing apoptosis of human breast carcinoma cells SK-BR-3 and the possible mechanism.</p><p><b>METHODS</b>MTT assay was used to detect the growth inhibition induced by 3-BrPA in breast cancer cells SK-BR-3. The apoptotic cells were detected by flow cytometry with propidium iodide (PI). ATP levels in the cells were detected by ATP assay kit, and DHE fluorescent probe technique was used to determine superoxide anion levels; the mitochondrial membrane potential was assessed using JC-1 staining assay.</p><p><b>RESULTS</b>MTT assay showed that the proliferation of SK-BR-3 cells was inhibited by 3-BrPA in a time- and concentration-dependent manner. Exposure to 80, 160, and 320 µmol·L(-1) 3-BrPA for 24 h resulted in cell apoptosis rates of 6.7%, 22.3%, and 79.6%, respectively, and the intracellular ATP levels of SK-BR-3 cells treated with 80, 160, 320 µmol·L(-1) 3-BrPA for 5 h were 87.7%, 60.6%, and 23.7% of the control levels. 3-BrPA at 160 µmol·L(-1) increased reactive oxygen levels and lowered mitochondrial membrane potential of SK-BR-3 cells.</p><p><b>CONCLUSION</b>3-BrPA can inhibit cell proliferation, reduce the mitochondrial membrane potential and induce apoptosis in SK-BR-3 cells, the mechanism of which may involve a reduced ATP level by inhibiting glycolysis and increasing the reactive oxygen level in the cells.</p>

Small interfering RNA-mediated RIP1 knockdown enhances L-OHP sensitivity of human oral squamous carcinoma cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of small interfering RNA-mediated receptor-interacting protein kinase 1 (RIP1) knockdown on the sensitivity of human oral squamous carcinoma cells to to oxaliplatin (L-OHP)-induced apoptosis and explore a new target for clinical treatment of oral squamous carcinoma.</p><p><b>METHODS</b>The viability of human oral squamous carcinoma cell line KB exposed to different concentrations (0, 0.25, 0.5, 1, 2, 4 µmol/L) of L-OHP were detected by MTT assay. PI/Annexin V staining was used to observe cell apoptosis in naive KB cells, cell and transfected with pSH1Si-RIP1 or with the empty plasmid. Western blotting was used to detect RIP1 expression in KB cells exposed to L-OHP and in cells transfected with pSH1Si-RIP1.</p><p><b>RESULTS</b>Exposure to L-OHP (1µmol/L) for 24, 48, 72 h resulted in KB cell survival rates of 67.66%, 55.17%, and 41.34%, respectively, but the cell apoptosis rate was only 9.6% following a 24-h exposure. KB cells transfected with pSH1Si-RIP1 showed an apoptotic rate of 9.4%, which increased to 29.1% following L-OHP exposure. RIP1 expression was first up-regulated and then down-regulated in KB cells treated with L-OHP, and was significantly reduced after cell transfection with pSH1Si-RIP1.</p><p><b>CONCLUSION</b>Suppression of RIP1 expression increases the apoptotic rate of human oral squamous carcinoma cells, suggesting the potential of RIP1 as a new candidate target for clinical treatment of oral squamous carcinoma.</p>

Glycosylation inhibitor 2-deoxy-D-glucose sensitizes oral cancer cells to TRAIL-induced apoptosis / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of 2-deoxy-D-glucose (2-DG) in enhancing the sensitivity of oral cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis.</p><p><b>METHODS</b>The oral cancer cell line KB was incubated in the presence of different concentrations (0, 0.625, 1.25, 2.5, 5, and 10 mmol/L) of 2-DG with or without TRAIL (200 ng/ml). The cell viability was measured using MTT assay and cell apoptosis was detected using flow cytometry with propidium iodide (PI) staining. KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3.</p><p><b>RESULTS</b>Treatment of the cells with 5 mmol/L 2-DG for 24, 48 and 72 h resulted in a cell viability of 25.25%, 69.06%, and 59.19%, respectively. Combined treatment with 5 mmol/L 2-DG with TRAIL for 24 significantly enhanced the cell apoptotic rate (72.5%) as compared to the rate induced by TRAIL alone (45.3%) and by 2-DG (15.9%) alone. 2-DG treatment markedly up-regulated DR5 and caspase-3 expression and enhanced the inhibitory effect of TRAIL on cell colony formation.</p><p><b>CONCLUSION</b>2-DG sensitizes oral cancer cells to TRAIL- induced apoptosis by up-regulating DR5 and caspase-3 expressions.</p>

Small interfering RNA-mediated glucose-regulated protein 78 knockdown enhances chemosensitivity of breast cancer cells to cisplatin / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of small interfering RNA-mediated glucose-regulated protein 78 (GRP78) knockdown on the chemosensitivity of breast cancer cells to cisplatin.</p><p><b>METHODS</b>Human breast cancer cell line MDA-MB-231 was exposed to different doses of cisplatin (0, 1, 2, 4, 8, and 16 µmol/L), and the changes in cell viability were detected using MTT assay. PI/Annexin V staining was used to observe the apoptosis of the cells in response to transfection with a small interfering RNA targeting GRP78 (pSH1Si-GRP78). Western blotting was employed to detect GRP78 expression in pSH1Si- GRP78-transfected cells after exposure to 8 µmol/L cisplatin for 24, 48 and 72 h.</p><p><b>RESULTS</b>Exposure of the cells to 8 µmol/L cisplatin for 24, 48 and 72 h resulted in a cell survival rate of 83.13%, 54.22% and 35.79%, respectively, but the cell apoptosis rate was only 10.8% at 24 h. Transfection of MDA-MB-231 cells with pSH1Si-GRP78 caused a cell apoptosis rate of 24.6%, which increased to 48.9% in cells with both pSH1Si-GRP78 transfection and cisplatin exposure. Cisplatin exposure caused an initial up-regulation followed then by a down-regulation of GRP78 expression in MDA-MB-231 cells, while pSH1Si-GRP78 transfection produced an obvious down-regulation of GRP78 expression.</p><p><b>CONCLUSIONS</b>Inhibition of GRP78 expression increases the apoptosis and enhance cisplatin chemosensitivity of breast cancer cells in vitro, suggesting the value of GRP78 as a potential therapeutic target in the clinical treatment of breast cancer.</p>

Effects of cisplatin combined with heparanase inhibitor on proliferation and invasion of human nasopharyngeal carcinoma cells / 药学学报

This study is to investigate the effects of cisplatin combined with heparanase inhibitor OGT2115 on proliferation, invasion and migration of human nasopharyngeal carcinoma cells CNE-2 and to provide a new target for the treatment of metastasis of nasopharyngeal carcinoma. MTT assay was used to detect the cell viability of CNE-2 after exposure to different concentrations of DDP (2, 4, 8, 16 and 32 micromol x L(-1)), different concentrations of OGT2115 (0.4, 0.8, 1.6, 3.2 and 6.4 micromol x L(-1)), and DDP combined with OGT2115. Transwell assay was applied to analyze the effects of drugs on invasion and migration of human nasopharyngeal carcinoma cells. Wound healing assay was performed to detect cell migration and heparanase activity was analyzed by ELISA. MTT results showed that DDP can inhibit the proliferation of CNE-2 cells in a time and concentration-dependent manner, with an IC50 of 24.03 micromol x L(-1) at 24 h (P < 0.05), low concentration of DDP has almost no inhibitory effect on cell invasion and migration. DDP combined with OGT2115 can significantly inhibit cell invasion and migration. Inhibition of heparanase can significantly enhance anti-invasion and anti-proliferation of DDP.

Effect of tunicamycin combined with cisplatin on proliferation and apoptosis of human nasopharyngeal carcinoma cells in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effects of tunicamycin (a glycosylation inhibitor) combined with cisplatin on the proliferation and apoptosis of human nasopharyngeal carcinoma cells and explore the molecular mechanism.</p><p><b>METHODS</b>Nasopharyngeal carcinoma CNE-1 and CNE-2 cells cultured in vitro were treated with different concentrations of tunicamycin with or without cisplatin. The inhibition of cell proliferation was examined using MTT assay and colony formation assay, and the cell apoptosis was analyzed using flow cytometry with propidium iodide staining. The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 µmol/L tunicamycin with or without 6.00 µmol/L cisplatin were measured with Western blotting.</p><p><b>RESULTS</b>Treatment with tunicamycin or cisplatin obviously inhibited the proliferation of CNE-1 and CNE-2 cells. Treatment with 3 µmol/L tunicamycin for 24, 36 and 48 h resulted in a viability of 72.13%, 51.97%, and 37.56% in CNE-1 cells and 85.61%, 56.95%, and 43.66% in CNE-2 cells, respectively, and the combined treatment with 6 µmol/L cisplatin lowered the cell viability to 67.97%, 47.76%, and 34.68% in CNE-1 cells and 56.89%, 37.05%, and 29.30% in CNE-2 cells, respectively. Tunicamycin at 0.3 µmol/L combined with 0.6 µmol/L cisplatin showed an obviously enhanced inhibitory effect on colony formation of CNE-1 and CNE-2 cells. Tunicamycin treatment (3 µmol/L) of CNE-1 and CNE-2 cells for 48 h induced an apoptosis rate of only 8.89% and 8.67%, but when combined with 6 µmol/L cisplatin, the cell apoptosis rate increased to 37.02% and 32.25%, significantly higher than that in cells with cisplatin treatment alone (7.25% and 6.36%, respectively). Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3.</p><p><b>CONCLUSION</b>Tunicamycin can inhibit the proliferation of CNE-1 and CNE-2 cells and enhance cisplatin-induced cell death, the mechanism of which may involve excessive endoplasmic reticulum stress response and increased activity of caspase-3.</p>

Effect of low-molecular-weight heparin combined with paclitaxel on the invasiveness and migration of nasopharyngeal carcinoma cells in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of low-molecular-weight heparin (LMWH) combined with paclitaxel (PTX) on the invasiveness and migration of nasopharyngeal carcinoma cells and explore the molecular mechanisms.</p><p><b>METHODS</b>MTT assay was used to detect the growth inhibition induced by LMWH and PTX in CNE1 and CNE2 cells. Wound healing assay and Transwell migration assay were employed to assess the effects of the drugs on the cell migration, and Transwell invasion assay was used to evaluate the cell invasiveness. The cellular expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were analyzed by Western blotting. ELISA was used to determine the expression of heparanase (HPA) in the culture medium of the cells.</p><p><b>RESULTS</b>MTT assay showed an obvious suppression of CNE1 and CNE2 cell proliferation in response to LMWH and PTX treatments. Treatment with 200 U·ml LMWH combined with 0.1 µmol·L PTX for 24 h resulted in the inhibition rates of migration of 66.70% and 70.53% in CNE1 and CNE2 cells, respectively significantly higher than the rates in cells with PTX treatment alone. The combined treatment with LMWH and PTX for 24 h also caused a significantly higher inhibition rate of cell invasion than LMWH and PTX alone. LMWH enhanced the down-regulation of MMP-9 and HPA induced by PTX.</p><p><b>CONCLUSION</b>LMWH can enhance the inhibitory effect of PTX on the migration and invasion of nasopharyngeal carcinoma cells, the mechanism of which may involve the down-regulation of MMP-9 and HPA expressions.</p>

The Regulation of Histone Modifications / 生物化学与生物物理进展

Epigenetics refers to non-coding sequence changes such as DNA methylation, histone modifications, chromosome remodeling and non-coding RNA regulation.Histone modifications include acetylation, phosphorylation, methylation, ubiquitination and ADP ribosylation.The combinations of different histone modifications, known as "histone code", are dynamic during development and differentiation and play important roles in the regulation of gene expressions in spatial-temporal manners.The modification on a particular residue in a histone affects not only the modifications at different residues in its own protein but also other histones.The histone modifications is a complicated network and the regulation remains elusive.

Time course and distribution of myocyte apoptosis induced by acute ischemia in rats / 中国病理生理杂志

AIM: Myocyte apoptosis in rats can be induced by acute ischemia, but time course and distribution of myocyte apoptosis were unclear.METHODS:DNA agarose gel electrophoresis and TdT-mediated dUTP nick end-labling(TUNEL) assay were performed to evaluate apoptosis in mycardium exposed to 45 minutes, 2 hours, 6 hours, 12 hours ischemia and sham-operated rats in vivo.RESULTS: DNA ladders were clearly visible in agarose gel of DNA from ischemic myocardium exposed to 2 hours, 6 hours and 12 hours ischemia, and DNA ladders became more apparent with increasing duration of ischemia. TUNEL positive cells with apoptotic morphologic characters were present in above ischemia time, and apoptotic index increased with increasing ischemia time. The majority of TUNEL positive cells were myocytes. Apoptotic index was higher in subendocardium than in subepicardium(P

Inhibitory effects of heparan sulfate proteoglycan on transplanted breast cancer in C_3H mice / 中国药理学通报

Aim To observe the anti-tumor activity and the mechanism of heparan sulfate proteoglycan(HSPG) on C3H mice transplanted tumors.Methods Tumor model was established and randomly divided into five groups.HSPG groups(5,10,50 mg?kg-1),positive group and control group,intraperitoneal injection was performed once a day for 22 days and the volume of tumors was measured.Mice were treated on 24th day,then tumor weight was examined,thymus index,and spleen index were calculated,the apoptosis was determined by TdT-mediated Dutp nick end labeling(TUNEL) assay in situ,the expression of vascular endothelial growth factor(VEGF) was detected by immunohistochemistry.Results The tumor volume in HSPG groups was reduced without the decrease of thymus index,spleen index.TUNEL assay in situ showed numerous heavy blue apoptosis cells in the HSPG groups significantly higher than in control groups.The tumors in HSPG groups showed significantly lower VEGF expression than those in control group.Conclusion HSPG had significant anti-tumor effects on C3H mice transplantable breast cancer.The mechanisms may be associated with the effects of inducing tumor cell apoptosis and inhibiting the VEGF expression.

Inhibition of MEK sensitizes human breast carcinoma cells to endoplasmic reticulum pathway's apoptosis / 中国药理学通报

Aim To investigate the inhibition of MEK/ERK pathway affecting the sensitivity of human breast carcinoma cells SK-BR-3 to endoplasmic reticulum(ER) stress-induced apoptosis and wish to find new targets for human breast carcinoma chemotherapy.Methods Different concentrations(0,1.5,3,6,9 and 12 ?mol?L-1) tunicamycin(TM) treated human breast carcinoma cells SK-BR-3 for 48 h,then propidium iodide(PI) staining measured apoptotic cells in Flow Cytometry(FCM).Different times(0,6,12,24 and 36 h) of TM(3 ?mol?L-1) treated SK-BR-3 cells,Western blot measured proteins GRP78,ERK1/2 and pERK expression.MEK inhibitor U0126(20 ?mol?L-1) pretreated cells for 1 h before treatment with TM(3 ?mol?L-1) in different concentrations and times,measured above identical indexes and compared with their diversities of treatment with U0126 or not.Results TM induced apoptotic cells