Comparison on the effects of three sex hormones on the fetal rat calvarial osteoblasts

Despite the overwhelming evidence of estrogenin bone preservation in postmenopausal osteoporosis, the mechanism of action of sex hormones onbone metabolism remains uncertain. In order toexplore the effect of 178--estradiol (E, ), progesterone (P ), and testosterone (T ) on rat osteoblasts proliferation and differentiation and difference of actions of these hormones, rat calvarialosteoblasts were used as culture model, since thisculture system, when cultured in a suitable environment, could mim…     

不同糖浓度对颌骨骨髓间充质干细胞成骨分化的影响

目的 研究不同糖浓度对颌骨骨髓间充质干细胞（orofacial bonemesenchymal stem cells, OFMSCs）增殖和成骨分化的影响。方法 体外分离、培养OFMSCs,成骨、成脂、成软骨分化诱导及鉴定,并使用不同含糖量培养基（5.5、11、16.5、25、44 mmol/L）培养OFMSCs,以5.5 mmol/L基准糖浓度为对照组,其余组为实验组。采用CCK-8及流式细胞仪检测各组OFMSCs的增殖活性及增殖指数,OFMSCs成骨诱导后4、7 d检测碱性磷酸酶（ALP）活性,21 d进行茜素红染色及矿化定量分析,同时用RT-PCR检测3、7、14及21 d相关成骨基因Runx2、Osterix的表达。结果 培养的OFMSCs成骨诱导21 d后茜素红染色可见钙结节,成脂诱导14 d 后油红O染色可见红色脂滴,成软骨诱导14 d 后阿利新蓝染色可见蓝色胞浆;糖浓度在5.5～25 mmol/L促进OFMSCs的增殖,但随着糖浓度的继续增加（25～44 mmol/L）,OFMSCs的增殖活性受抑制;成骨诱导时,随着培养液糖浓度升高,ALP活性呈剂量依赖性降低（P Runx2、Osterix mRNA 表达量高于实验组（P Runx2、Osterix mRNA 表达量均出现先上调再下调的趋势。结论 在一定范围的糖浓度内,糖浓度升高可促进OFMSCs的增殖;而糖浓度升高对成骨分化呈抑制效应。     

siRNA沉默HLX基因对AML细胞生长的影响

目的 筛选高表达H2.0样同源盒基因（H2.0-like homeobox gene,HLX）的白血病细胞株,沉默HLX后观察急性髓系白血病（acute myelogenous leukemia,AML）细胞株的生长及分化影响,为HLX在AML中的深入研究提供理论基础。方法 实时荧光定量PCR（quantitative real-time polymerase chain reaction,qRT-PCR）筛选高表达HLX基因的白血病细胞株,并检测p21活化激酶1（p21-activated kinase 1,PAK1）的基因表达;设计siRNA-HLX沉默HLX基因表达最高的AML细胞株中的该基因,运用相差显微镜观察细胞生长情况,MTS/PMS比色分析法检测增殖抑制率。结果 AML细胞株中HLX基因的表达水平显著较高（P< 0.01）,干扰HLX基因后,可见AML细胞株生长速度减慢,增殖被抑制,并且PAK1mRNA表达下调（P< 0.01）。结论 HLX基因可抑制AML细胞株的生长、增殖及分化。     

Wild-type smad3 gene enhances the osteoblastic differentiation of rat bone marrow-derived mesenchymal stem cells in vitro

Summary This study examined the effect of wild-type Smad3 gene on the osteoblastic differentiation of rat bone marrow-derived mesenchymal stem cellsin vitro. Bone marrow-derived mesenchymal stem cells (MSCs) were stably transfected with the complexes of pcDNA3. 0-Myc-Smad3 or pcDNA3. 0-Myc-Smad3ΔC and Lipofectamine reagent. Immunofluorescence staining was performed to evaluate the c-Myc signal in MSCs. The cell proliferation was detected by MTT method. To clarify the osteoblastic characteristics in stably transfected MSCs, alkaline phosphatase (ALP) mRNA and core binding factor α1 (Cbfa1) mRNA were investigated by RT-PCR, and ALP activity and mineralization were examined by p-nitrophenolphosphate method and alizarin red staining respectively. PD98059, a specific inhibitor of the ERK signaling pathway, was used to determine the role of ERK in Smad3-MSCs osteoblastic differentiation. c-Myc signal was detected in Smad3-MSCs and Smad3 ΔC-MSCs. The proliferation of Smad3-MSCs was slower than that of Smad3 ΔC-MSCs or V-MSCs. The relative levels of ALP mRNA and Cbfal mRNA in Smad3-MSCs, as well as ALP activity and mineralization, were markedly higher than those in Smad3 ΔC-MSCs or V-MSCs. Although ALP activity and mineralization were slightly lower in Smad3-MSCs treated with PD98059 than in those without PD98059 treatment, no significant difference was found between them (P>0.05). It is concluded that the wild-type Smad3 gene, which is a crucial component promoting bone formation, can inhibit the proliferation of MSCs and enhance the osteoblastic differentiation of uncommitted MSCs and the maturation of committed MSCs independent of the ERK signaling pathway. ZHENG Qixin, male, born in 1952, Professor This study was supported by a grant from the National Natural Science Foundation of China (No. 30170270).     

Experimental Study on the Inhibitory Effects of Verapamil on the Proliferation of Meningiomas Cells

In order to investigate the effects of verapamil on the proliferation of meningiomas cells in vitro and in vivo, the cultured meningiomas cells were cultured with verapamil at different concen-trations for 24 h and the inhibitory effects of verapamil on cell proliferation were observed by MTT method. The meningiomas model was established by implanting the newly removed tumor fragments into the nude mice subcutaneously. The nude mice with tumors were divided into two groups: vera-pamil-treated group and control group. Tumor volumes were measured and after 12 weeks the tumors were taken out and examined histologically. The expression of proliferating cell nuclear antigen (PCNA) in the tumors was detected by using immunohistochemistry. It was found that verapamil could inhibit the growth of cultured meningiomas cells in a concentration-dependant manner. The in-hibitory effect could be observed in the concentration of 1 μmol/L verapamil and the most obvious effects appeared in the concentration of 100 μmol/L. Tumor volume in the verapamiltreated group was obviously smaller than that in the control group (211.40±5.50 vs 163.94±3.62, P<0.01) and the expression of PCNA was also lower (1.52±0.24 vs 2.86±0.53, P<0.05). Tumor inhibition rate was about 22.45%. It was suggested that verapamil could inhibit the proliferation and growth of men-ingiomas cells in vitro and in vivo.     

Effects of retinoic acid on the β-catenin/TCF pathway in culture porcine tracheobronchial epithelial cells

Summary The effects of retinoic acid on the β-catenin/TCF pathway in cultured porcine tracheo-bronchial epithelial cells (TBEC) were investigated. After TBEC were treated with retinoic acid at various concentrations, mRNA and protein changes of β-catenin in cytoplasm, nucleus and whole cell of the TBEC were observed by immunocytochemical stain, RT-PCR and Western blotting. And the changes of the target gene cyclinD1 of β-catenin/TCF pathway were also observed. It was found that there was no significant difference in β-cat mRNA level after retinoic acid treatment. However, the expression of β-catenin in the whole cell and cytoplasm was elevated with the increase of retinoic acid concentration (P<0.01). The nuclear protein β-catenin and target gene cyclinD1 of β-catenin/TCF pathway was decreased (P<0.05). It was indicated that retinoic acid could increase β-catenin level of the whole cell protein and decreased nuclear β-catenin, downregulating β-cat/TCF signaling activity and reducing target gene cyclinD1 protein level. As a result, retinoic acid can downregulate β-catenin/TCF pathway in porcine tracheobronchial epithelial cell, suggesting that retinoic acid can inhibit the proliferation and accelerate differentiation of tracheobronchial epithelial cells. Li Yuan, female, born in 1977, Assistan: This project was supported by a grant from National Natural Sciences Foundation of China for youth scientist (No. 30200115).     

Effect of rhBMP-2 and Osteogenic Revulsants on Proliferation and Differentiation of Bone Marrow Stromal Cells in Rats

The effects of recombinant human bone morphogenetic protein-2 （rhBMP-2） and osteogenic revulsants alone or in combination at different time points and in different dosages on proliferation and osteogenesis of bone marrow stromal cells （BMSCs） in SD rats were investigated. Rat BMSCs were cultured in vitro and induced by rhBMP-2 in different dosages （10, 50, 100 and 200μg/L） alone or in combination with osteogenic revulsants. MTT colorimetric assay was used to evaluate The proliferation, activity of alkaline phosphoric （ALP） and osteocalcin were measured at 3rd, 6th, 9th, 12th day respectively. The results showed that rhBMP-2 and osteogenic revulsants could promote the differentiation of BMSCs towards osteoblast phenotype. The proliferation of BMSCs could be enhanced by rhBMP-2 in a dose-dependent manner. The expression of osteoblast phenotype was significantly higher by using both of them than by using them alone, which was verified by the activity of ALP and osteocalcin. It was suggested that the combined use of rhBMP-2 and osteogenic revulsants could promote the proliferation and simultaneously induce and maintain the expression of osteoblast phenotype of BMSCs in rats.     

Expression and biological function of N-myc down-regulated gene 1 in human cervical cancer

The expression of N-myc down-regulated gene 1 (NDRG1) has previously been reported to be involved in the proliferation,differentiation,invasion and metastasis of cancer cells,but its role in cervical cancer is still unclear.This study aimed to investigate the expression of NDRG1gene in human cervical cancer and its effect on aggressive tumor behaviors.The NDRG1 expression in cervical tissues and cells was detected by RT-PCR.Specific expression plasmid pEGFP-N1-NDRG1-GFP was used to enhance the expression of NDRG1 in human cervical cancer cell lines.The mRNA and protein level of NDRG1 was assessed by RT-PCR and Western blotting,respectively.Its effects on cell proliferation,migration,invasion,cell cycle and apoptosis were detected by MTT,transwell migration assay and flow cytometry (FCM),respectively.The results showed that the expression of NDRG1 in cervical cancer tissues and cells was significantly lower than in normal cervical tissues (P<0.001).After transfection with pEGFP-N1-NDRG1-GFP,the mRNA and protein expression of NDRG1 was up-regulated in Siha cells,which suppressed cell proliferation (P<0.001),induced cell cycle arrest (P<0.05),reduced invasion and migration of Siha cells (P<0.05),but caused no cell apoptosis.Moreover,vascular endothelial growth factor (VEGF),a tumor-induced angiogenesis factor,was markedly reduced and E-cadherin,a cell adhesion molecule,was increased in the cells transfected with pEGFP-N1-NDRG1-GFP.It was concluded that up-regulated NDRG1 may play a role in the suppression of malignant cell growth,invasion and metastasis of human cervical cancer.     

Effects of Peptide Nucleic Acids against Ki-67 Gene on the Proliferation and Apoptosis of Human Renal Carcinoma Cell Line

Ki-67 antigen is a DNA-binding protein which is an absolute requirement for proliferation of tumor cells[1]. Since transformation of malignant cells is frequently associated with high cell proliferation and proliferation is closely associated with the Ki-67 protein labeling index, this protein may serve as a potential target for cancer therapy although a causative involvement of Ki-67 ex-pression has not been conclusively demonstrated so far. PNAs are synthetic structure homologues of antise…     

Stathmin与妇科肿瘤的研究进展

Stathmin蛋白由于其特有的微管解聚活性,在细胞的增殖和分化及肿瘤发生中发挥着十分重要的作用。多种恶性肿瘤中Stathmin都有高水平表达,抑制其表达可以干扰恶性细胞的增殖。目前已经证实,Stathmin的过表达能够影响某些作用于微管化疗药物的疗效,对指导临床用药有一定的意义。Stathmin为肿瘤基因治疗提供了一个分子新靶点。Stathmin在妇科肿瘤方面的研究目前尚不多见。现就Stathmin的分子结构、生物学功能、作用机制及其与妇科肿瘤的关系进行综述。     

血小板浓缩生长因子对人牙髓细胞存活及其增殖分化的影响

目的 探讨血小板浓缩生长因子(Concentrate Growth factors,CGF) 对人牙髓细胞(human dental pulp cells,hDPCs)增殖分化的影响,为其今后在牙髓及根尖周疾病治疗应用进行前期研究。方法 从因正畸治疗拔除的健康恒牙分离培养出人牙髓细胞,在体外采用CGF或矿物三氧化物聚合体(mineral trioxide aggregate, MTA)处理人牙髓细胞,分别在第1、3、7天,CCK-8法测定各组细胞增殖水平、碱性磷酸酶活性、流式细胞术检测细胞周期和细胞凋亡情况。结果 与MTA组相比,CGF组的细胞增殖能力增强,S期细胞的比例增加,且第3、7天ALP活性增高（P<0.05）, 而第1、7天牙髓细胞凋亡率降低。结论 CGF在体外具有良好的促进牙髓细胞增殖,抗凋亡以及诱导成骨/成牙分化的能力。     

Blocking Ihh signaling pathway inhibits the proliferation and promotes the apoptosis of PSCs

Summary： The roles of Indian hedgehog （Ihh） signaling pathway in the proliferation and apoptosis of precartilaginous stem cells （PSCs） were investigated. PSCs, labeled with fibroblast growth factor receptor 3 （FGFR-3）, were isolated from neonatal rats by immunomagnetic separation. After identification with FGFR-3 and Col II, the cells were incubated with different concentrations of cyclopamine （cyclo）, the specific inhibitor of Ihh signaling pathway. The morphologic changes of the cells were observed under the inverted phase contrast microscope. The mRNA expression levels of Ihh, parathyroid hormonerelated peptide （PTHrP）, protein Patched （Ptch）, Bcl-2 and p21 were detected by RT-PCR. The protein expression levels of Ihh and Ptch were measured by Western blot. MTT assay was used to examine the effects of cyclo on proliferation of PSCs. Apoptosis rate of PSCs was examined by AnnexinV/PI assay of flow cytometric analyses. After PSCs were incubated with cyclo, obvious morphologic changes were observed as compared with the control group. The mRNA expression levels of PTHrP, Ptch and Bcl-2 were decreased to varying degrees in a cyclo dose-dependent manner. However, the expression levels of Ihh and p21 mRNA were increased. The protein expression of Ptch and Ihh had the same change as the mRNA expression. Meanwhile, cyclo could obvi- ously inhibit the proliferation and promote the apoptosis of PSCs. The results indicated that Ihh signaling pathway plays an important role in regulating the proliferation and apoptosis of PSCs, which is probably mediated by Bcl-2 and p21.     

补肾壮骨方剂含药血清调控牙周膜干细胞增殖分化的效能研究

目的：探讨补肾壮骨方剂含药血清对人牙周膜细胞增殖和骨向分化的作用。方法采用酶消化法体外培养人牙周膜细胞,用不同剂量的补肾壮骨方剂含药血清处理细胞,通过四唑盐（ MTT）比色试验和碱性磷酸酶活性测试,检测补肾壮骨方剂含药血清对细胞体外增殖分化的影响。结果体外实验补肾壮骨方剂含药血清对人牙周膜细胞增殖有明显促进作用,且能促进人牙周膜细胞碱性磷酸酶的活性表达。结论补肾壮骨方剂含药血清促进牙周膜细胞的增殖活性,可明显促进牙周膜细胞骨向分化。     

Let-7d通过靶向调控Rhotekin基因抑制骨肉瘤细胞的增殖、迁移和侵袭

目的 探讨let-7d在骨肉瘤组织中的表达,并研究let-7d及其靶基因对人骨肉瘤细胞U2OS增殖、迁移和侵袭的影响。方法 收集2010年至2015年于我科行手术切除的25例骨肉瘤患者的肿瘤组织和癌旁组织（距肿瘤组织边缘>5 cm）,并用qPCR检测let-7d的表达情况。构建稳定过表达let-7d的U2OS细胞,用qPCR验证let-7d过表达情况,以转染pCDH空病毒载体的U2OS细胞作为对照组细胞,并分别采用CCK-8实验、划痕实验和Transwell实验检测过表达let-7d对U2OS细胞增殖、迁移和侵袭能力的影响。通过微RNA靶基因预测软件和双荧光素酶实验明确let-7d的下游靶基因,检测过表达let-7d的U2OS细胞中靶基因的表达水平,并通过小干扰RNA技术研究抑制靶基因表达对U2OS细胞增殖、迁移和侵袭的影响。结果 骨肉瘤组织中let-7d表达水平低于癌旁组织（P<0.01）。与人成骨细胞hFOB1.19相比,U2OS细胞中let-7d表达水平下调（P<0.01）。与对照组相比,过表达let-7d能抑制U2OS细胞的增殖、迁移和侵袭（P均<0.05）。微RNA靶基因预测软件和双荧光素酶实验结果显示,Rhotekin（RTKN）基因是let-7d的直接靶基因,且过表达let-7d导致U2OS细胞中RTKN mRNA表达水平较对照组降低（P<0.01）。干扰RTKN表达能抑制U2OS细胞增殖、迁移和侵袭（P均<0.05）。结论 Let-7d通过靶向调控RTKN抑制骨肉瘤细胞的增殖、迁移和侵袭,可作为骨肉瘤治疗一个新的靶点。     

Effects of ghrelin on the proliferation and differentiation of 3T3-L1 preadipocytes

The effects of ghrelin on the proliferation and differentiation of 3T3-L1 preadipocytes and the possible mechanisms were investigated in this study. 3T3-L1 preadipocytes were cultured in vitro and treated with different concentrations of ghrelin. Proliferation of 3T3-L1 preadipocytes was evaluated by MTT method and mRNA levels of c-myc and thymidine kinase were detected by RT-PCR. Morphological changes of 3T3-L1 preadipocytes were observed and cell differentiation was measured by oil red O staining. The mRNA levels of peroxisome proliferator-activated receptor γ （PPARγ） and CAAT/enhancer binding protein （C/EBPa） in the cells at different differentiation stages were detected by RT-PCR. The results showed that ghrelin at concentrations of 10^-7 to 10^-15 mol/L could significantly promote preadipocyte proliferation （P〈0.05）, with the most pronounced effect observed at 10^-11 mol/L （P〈0.01）. Treatment of 3T3-L1 preadipocytes with ghrelin significantly increased the mRNA levels of c-myc and thymidine kinase （P〈0.01）. Morphological findings demonstrated that the great amount of lipid droplets appeared in the 3T3-L1 preadipocytes treated with ghrelin. Ghrelin could morphologically induce the differentiation of 3T3-L1 preadipocytes into mature adipocytes. Ghrelin significantly increased the mRNA levels of PPAR7 and C/EBPα during the differentiation, when compared with control group （P〈0.05）. The mRNA levels of PPARγ and C/EBPα were obviously up-regulated with the differentiation of preadipocytes after the treatment of ghrelin. There were significant difference in the mRNA levels of PPARγ and C/EBPu on day 2 and day 8 of the differentiation of 3T3-L1 preadipocytes （P〈0.01）. In conclusion, ghrelin could promote the proliferation and differentiation of 3T3-L1 preadipocytes by increasing the mRNA levels of PPARγ and C/EBPα and therefore enhance the sensitivity of adipocytes against insulin.     

乏氧环境下骨骺干细胞株在软骨载体中的相容性、增殖和分化成软骨的实验研究

目的观察乏氧环境中转染PTHrP基因的骨骺干细胞株在不同浓度HIF-1作用下与组织工程软骨载体材料的相容性,以及在软骨载体材料中骨骺干细胞株的增殖、分化成软骨作用。方法乏氧环境中,携带骨骺干细胞株的软骨载体置于含不同浓度HIF-1(0、20、40、80、100、120、140及160 pmol/L)的培养诱导液中培养,MTT法检测骨骺干细胞在载体上的黏附率及骨骺干细胞增殖情况;骨骺干细胞经转化生长因子1(TGF-1)诱导2周后免疫组化检测Ⅱ型胶原(collagenⅡ)、Aggrecan软骨蛋白聚糖表达情况;诱导后的骨骺干细胞与载体复合培养后4周取材电镜下行组织学观察软骨结节形成情况。结果细胞在载体上黏附率90.5%;乏氧环境中HIF-1可促进骨骺干细胞增殖,增殖效应与HIF-1剂量有一定的依赖性;经TGF-1诱导2周后collagenⅡ、Aggrecan免疫组化染色阳性;诱导后的骨骺干细胞在载体内生长增殖良好,4周时可见新生类软骨样组织形成。结论乏氧环境下转染PTHrP基因的骨骺干细胞与载体具有良好的相容性;乏氧环境下HIF-1能促进骨骺干细胞株的增殖、分化成软骨,其促进作用有一定的剂量依赖性。     

Stathmin基因反义核酸对人成骨肉瘤细胞系的生长抑制作用

目的　探讨 Stathmin基因的反义核酸 (AS- ODN)对人成骨肉瘤细胞系的生长抑制作用 ,并观察与化疗药物合用后的协同作用 .方法　以高表达 Stathm in的人成骨肉瘤细胞系 SOSP- 96 0 7为靶细胞、反义 Stathmin(AS- ODN)为阻断剂 ,通过 MTT试验观察 AS- ODN对成骨肉瘤细胞的生长抑制作用及与紫杉醇 (PTX)的协同作用 ,流式细胞仪分析细胞增殖周期的影响 .结果　 AS- ODN及 AS- ODN与 PTX联合应用均明显抑制成骨肉瘤细胞的生长 (P <0 .0 5 ,P <0 .0 1) .SOSP- 96 0 7在 AS- ODN作用下 ,细胞分裂阻滞在分裂期的中期 ,并诱导细胞发生凋亡 .结论　 Stathmin基因的反义核酸(AS- ODN)对成骨肉瘤细胞的生长可能起十分重要的作用 ,它有望成为成骨肉瘤治疗的新靶点 ,与抗癌药联合应用有协同作用     

Effects of Panax notoginseng saponins on apoptosis induced by hydrogen peroxide in cultured rabbit bone marrow stromal cells via altering the oxidative stress level and down-regulating caspase-3

Objective

To investigate the effects of Panax notoginseng saponins (PNS) on hydrogen peroxide (H₂O₂)-induced apoptosis in cultured rabbit bone marrow stromal cells (BMSCs).

Methods

The effects of different concentrations of PNS on proliferation and early osteoblast differentiation of BMSCs were determined by the MTT assay and an alkaline phosphatase (ALP) assay. An optimal effective concentration of PNS was determined and used in subsequent experiments. The cultured BMSCs were divided into three groups: untreated control, H₂O₂ treated, and PNS pretreatment of H₂O₂ treated. The oxidative stress level was assessed by superoxide dismutase (SOD) and malondialdehyde (MDA) assays. Flow cytometry was used to determine BMSC apoptosis by staining with annexinV-FITC/propidium iodide (PI). The activity of caspase-3 enzyme was measured by spectrofluorometry.

Results

PNS (0.1g/L) significantly increased both BMSC proliferation rate and ALP activity, while it decreased the indicators of oxidative stress, caspase-3 activity, and the apoptosis rate of BMSCs induced by H₂O_2..

Conclusion

PNS, acting as a biological antioxidant, had a protective effect on H₂O₂-induced apoptosis in cultured rabbit BMSCs by decreasing oxidative stress and down-regulating caspase-3.     

microRNA干扰抑制MTDH的表达对乳腺癌细胞MDA-MB-231增殖和侵袭能力的影响

目的 探讨microRNA干扰技术沉默异黏蛋白（MTDH,metadherin蛋白）基因表达及对人乳腺癌细胞MDA-MB-231细胞增殖、转移、侵袭能力的影响。方法 将人工合成的针对MTDH基因的miRNA片段瞬时转染人乳腺癌细胞MDA-MB-231,通过Western blot法、RT-PCR法检测MTDH蛋白表达和MTDHmRNA;应用MTT检测法、划痕实验、Transwell实验检测抑制MTDH基因后对乳腺癌细胞增殖、转移、侵袭能力的影响。结果 MTDHmiRNA能有效抑制MTDH蛋白和MTDHmRNA表达,最佳抑制率分别为79.41%、80.56%（P<0.05）;经miRNA干扰的细胞,生长速度明显受到抑制（P<0.05）,侵袭迁移能力显著下降（P<0.05）。结论 MTDH miRNA瞬时转染人乳腺癌MDA-MB-231细胞可明显抑制癌细胞中MTDH表达,沉默MTDH基因表达后可明显抑制人乳腺癌MDA-MB-231细胞生长增殖、侵袭迁移能力。     

Effect of Smac on TRAIL-induced apoptosis of prostate cancer cell line PC-3 and the molecular mechanism

The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated. The Smac gene was transfected into PC-3 cells under the induction of liposome. The intrinsic Smac gene expression was detected by Western blotting. After treatment with TRAIL as an apoptosis inducer, in vitro cell growth activity was as-sayed by MTT colorimetry. The apoptosis rate of PC-3 cells was determined by annexin Ⅴ-FITC and propidium iodide staining flow cytometry. The expression of cellular XIAP and caspase-3 genes was examined by Western blotting. Smac-transfected cells (PC-3/Smac group) had significantly in-creased Smac protein level as compared with PC-3 controls (P<0.01). After induction with 100-200 ng/mL TRAIL for 12-36 h, cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P<0.05). After induction with 100 ng/mL TRAIL for 24 h, the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P<0.05). Ac-cordingly, the XIAP expression level was down-regulated significantly (P<0.05) and caspase-3 sub-unit P20 was up-regulated significantly (P<0.05). It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs), enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL, which may provide a useful experimental basis for prostate cancer therapy.