非培养表皮细胞对比毛囊滤泡细胞悬液移植治疗稳定型白癜风的Meta分析

目的 通过Meta分析评价非培养表皮细胞悬液移植(NECS)和毛囊滤泡细胞悬液移植(HFCS)对稳定型白癜风复色显效率。方法 由两位研究员独立利用计算机检索pubmed,Cochrane,Web of Science数据库,收集有关NECS和HFCS的相关文献并进行筛选,采用Cochrane系统评价员手册对文章质量进行评价以及Review Manager 5.4软件进行数据分析。结果 纳入6篇临床随机对照试验,均为英文文献。其中NECS104例,HFCS99例。结论 目前根据患者选择及显效率更倾向于NECS技术,但还需要更多的随机对照试验(Randomized Controlled Trial,RCT)研究进行比较。

骨髓间充质干细胞移植治疗猪急性心肌梗死疗效与机制的影像学评价

目的：将细胞生物学与PET、SPECT及MRI等影像检测手段结合，评价MSCs移植治疗模型猪缺血性心脏病的疗效并推测其机制。方法按随机数字表将24头猪[（25±5） kg]分为2组：MSCs移植组（ n＝12）及对照组（ n＝12）。建立AMI模型，体征平稳后于梗死周边心肌内注射自体MSCs（2×107，2 ml），对照组以相同方法注射等体积无血清Iscove改良的Dulbecc培养基（IMDM）培养液。 MSCs移植后1、4周时行PET及SPECT检测心肌葡萄糖代谢及心肌血流灌注情况，分别计算18 F？FDG平均信号强度（ MSI）、SRS、SRS百分比（ SRS％）等；采用MRI检测左心室功能，计算2组LVEF、ESV、左心室每搏输出量（ SV）及心输出量（ CO）等。4周时影像检测后处死动物，取心肌组织行HE及Masson染色。2组间比较采用非参数Mann？Whitney u检验，组内比较采用非参数Wilcoxon检验。结果（1）移植1周时MSCs移植组最低MSI低于对照组（22．10±3．18与35．70±3．02；z＝－2．65，P＜0．05），总MSI亦低于对照组（1013．50±29．37与1084．00±21．15；z＝－1．97，P＜0．05），其余指标2组间差异均无统计学意义。移植4周时，MSCs移植组最低MSI（34．00±4．25）较1周时明显提高（z＝－2．81， P＜0．01），总MSI（1075．50±28．30）亦明显提高（z＝－2．80，P＜0．01）；SRS及SRS％较1周时减低[20．20±2．24与23．80±1．58，（29．80±3．31）％与（35．10±2．34）％；均z＝－2．08，均P＜0．05]；左心室梗死区（MSI低于70的范围）内节段平均MSI较1周时明显增加（56．25±3．54与48．14±2．71；z＝－2．80，P＜0．01）。对照组上述参数4周时均较1周时改善，但差异均无统计学意义（均P＞0．05）。（2）移植1周时2组血流灌注参数无明显差异，4周时各血流灌注指标及灌注缺损范围均无明显改变。（3）移植1周时2组心功能参数无明显差异；移植4周时，MSCs移植组LVEF显著增加[（54．41±2．62）％与（47．54±2．43）％；z＝－2．60，P＜0．01]，ESV明显减低[（22．85±1．91）与（27．07±1．67） ml；z＝－2．70，P＜0．01），SV及CO较1周时均明显增加[（29．35±1．84）与（26．52±1．46）ml，（2．23±0．14）与（1．96±0．13） L／min；z＝－2．09和－1．99，均P＜0．05]；对照组未见明显差异（均P＞0．05）。结论经心肌内注射骨髓MSCs治疗猪急性心肌梗死，4周后心功能明显改善，心肌葡萄糖代谢显著提高，而心肌血流灌注未见明显改善；推测心功能的改善与心肌糖代谢增加有关。

Phase 1 human trial of autologous bone marrow-hematopoietic stem cell transplantation in patients with decompensated cirrhosis

AIM: To evaluate safety and feasibility of autologous bone marrow-enriched CD34+ hematopoietic stem cell Tx through the hepatic artery in patients with decompensated cirrhosis.METHODS: Four patients with decompensated cirrhosis were included. Approximately 200 mL of the bone marrow of the patients was aspirated, and CD34+ stem cells were selected. Between 3 to 10 million CD34+ cells were isolated. The cells were slowly infused through the hepatic artery of the patients.RESULTS: Patient 1 showed marginal improvement in serum albumin and no significant changes in other test results. In patient 2 prothrombin time was decreased; however, her total bilirubin, serum creatinine, and Model of End-Stage Liver Disease (MELD) score worsened at the end of follow up. In patient 3 there was improvement in serum albumin, porthrombin time (PT), and MELD score. Patient 4 developed radiocontrast nephropathy after the procedure, and progressed to type 1 hepatorenal syndrome and died of liver failure a few days later. Because of the major side effects seen in the last patient, the trial was prematurely stopped.CONCLUSION: Infusion of CD34+ stem cells through the hepatic artery is not safe in decompensated cirrhosis. Radiocontrast nephropathy and hepatorenal syndrome could be major side effects. However, this study doesnot preclude infusion of CD34+ stem cells through other routes.

Developmental pathways associated with cancer metastasis:Notch,Wnt,and Hedgehog

Master developmental pathways, such as Notch, Wnt, and Hedgehog, are signaling systems that control proliferation, cell death,motility, migration, and stemness. These systems are not only commonly activated in many solid tumors, where they drive or contribute to cancer initiation, but also in primary and metastatic tumor development. The reactivation of developmental pathways in cancer stroma favors the development of cancer stem cells and allows their maintenance, indicating these signaling pathways as particularly attractive targets for efficient anticancer therapies, especially in advanced primary tumors and metastatic cancers. Metastasis is the worst feature of cancer development. This feature results from a cascade of events emerging from the hijacking of epithelial-mesenchymal transition, angiogenesis, migration, and invasion by transforming cells and is associated with poor survival, drug resistance, and tumor relapse. In the present review, we summarize and discuss experimental data suggesting pivotal roles for developmental pathways in cancer development and metastasis, considering the therapeutic potential. Emerging targeted antimetastatic therapies based on Notch, Wnt, and Hedgehog pathways are also discussed.

Proliferation of L02 human hepatocytes in tolerized genetically immunocompetent rats

AIM: To investigate whether human hepatocytes could proliferate after transplantation to normal immunocompetent rats treated with 2-acetaminofluorene or Retrorsine and partial hepatectomy. METHODS: L02 hepatocyte-tolerant Sprague-Dawley rats were injected with Retrorsine, 2-acetaminofluorene or normal saline. L02 hepatocytes were then transplanted via the spleen. Human albumin and its mRNA, specific proliferating cell nuclear antigen (PCNA), L02 hepatocyte dynamic distribution, number density and area density of PCNA-positive cells in the liver were determined. RESULTS: All the examined indicators were not significantly different between the rats treated with 2-acetaminofluorene and normal saline, which was not the case with rats treated with Retrorsine. A dynamic distribution of L02 hepatocytes in the rat liver was detected from wk 1 to mo 6 after transplantation in the Retrorsine group and from wk 1 to 10 in the 2-acetaminofluorene group. Human albumin and its mRNA were detected from wk 2 to mo 6 in the Retrorsine group and from wk 1 to 8 in the 2-acetaminofluorene group. Specific human PCNA was detected in the rat liver from wk 2 to mo 6 in the Retrorsine group and from wk 2 to 6 in the 2-acetaminofluorene group. Human albumin and its mRNA contents as well as the number of PCNA positive cells reached a peak at wk 4. CONCLUSION: L02 human hepatocytes could not proliferate significiantly after transplantation to the normal, immunocompetent rats treated with 2-acetaminofluorene.L02 human hepatocytes can survive for 10 wk after transplantation and express human albumin for 8 wk. L02 human hepatocytes can proliferate and express human albumin for 6 mo after transplantation to the rats treated with Retrorsine. The chimeric L02 human hepatocytes, which then underwent transplantation into tolerant rats, were normal in morphogenesis, biochemistry and function.

Inhibitory effect of a new gossypol derivative apogossypolone (ApoG2) on xenograft of human prostate cancer cell line PC-3

Objective: To investigate the inhibitory effect of apogossypolone (ApoG2) on prostate cancer cell line PC-3 in vivo, and explore its mechanism. Methods: The models of transplantation tumors in Balb/c nu/nu mice were established via subcutaneous injection of PC-3 cells and the tumor-transplanted mice were divided into 4 groups: control group and three ApoG2 treatment groups, with 10 mice in each group. Volumes of the tumor were estimated every 2 d and the morphology of tumor tissues was observed. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and caspase-8 in tumor tissues. Results: ApoG2 (2.5 mg/kg-10 mg/kg) given intraperitoneally once a day can obviously inhibit the growth of subcutaneous prostatic carcinoma implant. The tumor volume decreased obviously when the treatment dosage was bigger than 5.0 mg/kg (P<0.01). Meanwhile, ApoG2 decreased the expression of PCNA and CD31, and enhanced the expression of caspases-3, caspase-8 in tumor tissues. Conclusion: ApoG2 exert an inhibitory effect on prostatic carcinoma possibly by inducing apoptosis and inhibiting tumor angiogenesis.

Glycation of high-density lipoprotein triggers oxidative stress and promotes the proliferation and migration of vascular smooth muscle cells

Background In type 2 diabetes mellitus （T2DM）, high-density lipoprotein （HDL） impairs its anti-atherogenic properties and even develops to a pro-inflammatory and pro-atherogenic phenotype because of abnormal compositions and modifications. In this study, we ex- amined the effects and the related mechanisms of glycation of HDL on the proliferation and migration of vascular smooth muscle cells （VSMCs）. Methods ＆ Results Glycated HDL （G-HDL） was modified with D-glucose （25 mmol/L） in vitro. Diabetic HDL （D-HDL） was isolated from T2DM patients. Rat VSMCs were isolated from the thoracic aortas. Human VSMCs were obtained from ScienCell Research Laboratories. Alpha-actin was detected through immunofiuorescence. VSMC proliferation was assayed by Cell Count. VSMC migration was determined by transwell chamber and scratch-wound assay. Intracellular reactive oxygen species （ROS） was detected based on ROS-medi- ated 2＇,7＇-dichlorofluorescein （DCFH-DA） fluorescence. Compared to native HDL （N-HDL）, G-HDL remarkably promoted VSMC prolif- eration and migration in the dose and time-dependent manners. In addition, G-HDL enhanced ROS generation in VSMCs. However, the ROS scavenger, N-acetylcysteine, efficiently decreased ROS production and subsequently inhibited the proliferation of VSMCs induced by G-HDL. Similarly, D-HDL from T2DM patients also promoted ROS release and VSMC proliferation and migration. Conclusions HDL either glycated in vitro or isolated from T2DM patients triggered VSMC proliferation, migration, and oxidative stress. These results might partly interpret the higher morbidity of cardiovascular disease in T2DM patients.

Nuclear reprogramming: the strategy used in normal development is also used in somatic cell nuclear transfer and parthenogenesis

Somatic cell nuclear transfer （SCNT） and parthenogenesis are alternative forms of reproduction and development, building new life cycles on differentiated somatic cell nuclei and duplicated maternal chromatin, respectively. In the preceding paper （Sun F, et al., Cell Res 2007; 17：117-134.）, we showed that an ＂erase-and-rebuild＂ strategy is used in normal development to transform the maternal gene expression profile to a zygotic one. Here, we investigate if the same strategy also applies to SCNT and parthenogenesis. The relationship between chromatin and chromatin factors （CFs） during SCNT and parthenogenesis was examined using immunochemical and GFP-fusion protein assays. Results from these studies indicated that soon after nuclear transfer, a majority of CFs dissociated from somatic nuclei and were redistributed to the cytoplasm of the egg. The erasure process in oogenesis is recaptured during the initial phase in SCNT. Most CFs entered pseudo-pronuclei shortly after their formation. In parthenogenesis, all parthenogenotes underwent normal oogenesis, and thus had removed most CFs from chromosomes before the initiation of development. The CFs were subsequently re-associated with female pronuclei in time and sequence similar to that in fertilized embryos. Based on these data, we conclude that the ＂erase-and-rebuild＂ process observed in normal development also occurs in SCNT and in parthenogenesis, albeit in altered fashions. The process is responsible for transcription reprogramming in these procedures. The ＂erase＂ process in SCNT is compressed and the efficiency is compromised, which likely contribute to the developmental defects often observed in nuclear transfer （nt） embryos. Furthermore, results from this study indicated that the cytoplasm of an egg contains most, if not all, essential components for assembling the zygotic program and can assemble them onto appropriate diploid chromatin of distinct origins.

Effects on Proliferation and Migration of the Human Colon Carcinoma Cell Line SW620 by Silencing of Hepatocyte Growth Factor Expression

OBJECTIVE Hepatocyte growth factor （HGF） expression is closely related to the progression and poor prognosis of colorectal cancer patients. In this study, we investigated the effects on proliferation and migration of the human colon carcinoma cell line SW620 by silencing HGF expression. METHODS HGF was silenced using specific HGF a/f3 siRNA. The proliferation, migration, cell cycle and ultrastructure of SW620 cells were examined. RESULTS The transfection efficiency was 70%-80%. The expression rate of HGF in the experimental group was significantly lower than that in the negative and blank control groups （P 〈 0.05）. The proliferation inhibition rate in the experimental group at 24, 48, 72 and 96 h after transfection was 14.2%, 50.2%, 39.5% and 23.2%, respectively. The migratory ability of cells in the experimental group was significantly inhibited compared with that in the negative control or blank control groups （58.2% vs. 2.1% or 0%, P 〈 0.05）. CONCLUSION The application of RNA interference to silence the expression of HGF in the colon carcinoma cell line SW620 effectively inhibits the proliferation and migration of tumor cells.

HGF/SF-Met signaling in tumor progression

Tumor progression is a multi-step process that requires a sequential selection of specific malignant phenotypes. Met activation may induce different phenotypes depending on tumor stage: inducing proliferation and angiogenesis in pri- mary tumors, stimulating motility to form micrometastases, and regaining the proliferation phenotype to form overt metastases. To study how HGF/SF-induced proliferative phenotypes switch to the invasive phenotype is important for understanding the mechanism of tumor progression and will provide an attractive target for cancer intervention and therapy.

Decreasing activity of NF-κB inhibits the proliferation of A549 cells via the down-regulation of cyclin D1 expression

Objective: To investigate the effect of decreasing activity of NF-κB on proliferation of A549 cell line and the pos-sible molecular mechanism. Methods: The recombinant plasmid PCDNA3.1(+)/IκBα expressing IκBα was constructed. The recombinant plasmid was then transfected to A549 cell. The activity of NF-κB, cell proliferation, and cyclin D1 expression were observed. Results: Our results showed that transfecting PCDNA3.1(+)/IκBα inhibited activity of NF-κB in A549 cells, and decreasing activity of NF-κB inhibited proliferation of A549 cells. Decreasing activity of NF-κB was accompanied with down-regulation of cyclin D1 expression. Conclusion: Decreasing activity of NF-κB inhibited proliferation of A549 cells, and the molecular mechanism of the inhibition effect may be down-regulation of cyclin D1 expression.

Local injection of liposomal adriamycin to inhibit metastatic cell proliferation in axillary nodes in rabbits bearing breast tumors

Objective: To assess the inhibitory effects of local injection of liposomal adriamycin (LADR) on the proliferation of lymph node metastases in rabbits bearing VX2 carcinoma in the mammary gland. Methods:Thirty female New Zealand white rabbits were divided into 3 groups, with 10 in each. VX2 tumor mass suspensions were injected into the breast tissues of rabbits. Treatment initiated once the axillary lymph node reached 5 mm in the maximum diameter. Group 1 received a sham treatment. Group 2 received a subcutaneous injection of LADR adjacent to tumor. Group 3 received an intravenous injection of free ADR (FADR) at the same dose and concentration to group 2. The breast tumors and axillary lymph nodes were resected after the treatment was repeated 3 times. The tumor and node sizes before and after treatment were measured. PCNA mRNA expressions in breast tumors and axillary nodes were determined using RT-PCR. Results: The mean growth ratios of lymph nodes after treatment were 3. 70, 1. 55, and 2. 89,respectively, in groups 1,2, and 3. The slowest node growth was observed in animals of group 2, with significant differences from group 1 (P<0. 001) and group 3 (P = 0. 002). The relative values of PCNA mRNA expression in lymph nodes were 0. 541, 0. 329,and 0. 450, respectively, in groups 1,2, and 3. Group 2 exhibited a significantly reduced PCNA mRNA expression in metastatic lymph node, as compared to group 1 (P<0. 001) and group 3 (P = 0. 004). Intravenous FADR injection effectively lowered the mRNA expressions of PCNA in breast tumors, which were not apparently altered after local LADR injection. Conclusion: Local injection of LADR holds a strong inhibitory effect on the proliferation of metastatic tumor cells in lymph nodes and appears to be an effective method for the treatment of lymphatic metastases of breast cancer.

High mobility group-box 3 overexpression is associated with poor prognosis of resected gastric adenocarcinoma

AIM:To elucidate high mobility group-box 3(HMGB3) protein expression in gastric adenocarcinoma,its potential prognostic relevance,and possible mechanism of action.METHODS:Ninety-two patients with gastric adenocarcinomas surgically removed entered the study.HMGB3 expression was determined by immunohistochemistry through a tissue microarray procedure.The clinicopathologic characteristics of all patients were recorded,and regular follow-up was made for all patients.The inter-relationship of HMGB3 expression with histological and clinical factors was analyzed using nonparametric tests.Survival analysis was carried out by Kaplan-Meier(log-rank) and multivariate Cox(Forward LR) analyses between the group with overexpression of HMGB3 and the group with low or no HMGB3 ex-pression to determine the prognosis value of HMGB3 expression on overall survival.Further,HMGB3 expression was knocked down by small hairpin RNAs(shRNAs) in the human gastric cancer cell line BGC823 to observe its influence on cell biological characteristics.The MTT method was utilized to detect gastric cancer cell proliferation changes,and cell cycle distribution was analyzed by flow cytometry.RESULTS:Among 92 patients with gastric adenocarcinomas surgically removed in this study,high HMGB3 protein expression was detected in the gastric adenocarcinoma tissues vs peritumoral tissues(P < 0.001).Further correlation analysis with patients' clinical and histology variables revealed that HMGB3 overexpression was obviously associated with extensive wall penetration(P = 0.005),a positive nodal status(P = 0.004),and advanced tumor-node-metastasis(TNM) stage(P = 0.001).But there was no correlation between HMGB3 overexpression and the age and gender of the patient,tumor localization or histologic grade.Statistical Kaplan-Meier survival analysis disclosed significant differences in overall survival between the HMGB3 overexpression group and the HMGB3 no or low expression group(P = 0.006).The expected overall survival time was 31.00 ± 3.773 mo(95%CI = 23.605-38.395) for patients with HMGB3 overexpression and 49.074 ± 3.648 mo(95%CI = 41.925-57.311) for patients with HMGB3 no and low-level expression.Additionally,older age(P = 0.040),extensive wall penetration(P = 0.008),positive lymph node metastasis(P = 0.005),and advanced TNM tumor stage(P = 0.007) showed negative correlation with overall survival.Multivariate Cox regression analysis indicated that HMGB3 overexpression was an independent variable with respect to age,gender,histologic grade,extent of wall penetration,lymph nodal metastasis,and TNM stage for patients with resectable gastric adenocarcinomas with poor prognosis(hazard ratio = 2.791,95%CI = 1.233-6.319,P = 0.019).In the gene function study,after HMGB3 was knocked down in the gastric cell line BGC823 by shRNA,the cell proliferation rate was reduced at 24 h,48 h and 72 h.Compared to BGC823 shRNA-negative control(NC) cells,the cell proliferation rate in cells that had HMGB3 shRNA transfected was significantly decreased(P < 0.01).Finally,cell cycle analysis by FACS showed that BGC823 cells that had HMGB3 knocked down were blocked in G1/G0 phase.The percentage of cells in G1/G0 phase in BGC823 cells with shRNA-NC and with shRNA-HMGB3 was 46.84% ± 1.7%,and 73.03% ± 3.51% respectively(P = 0.001),whereas G2/M cells percentage decreased from 26.51% ± 0.83% to 17.8% ± 2.26%.CONCLUSION:HMGB3 is likely to be a useful prognostic marker involved in gastric cancer disease onset and progression by regulating the cell cycle.

Changes of Ca^2+ activated potassium channels and cellular proliferation in autogenous vein grafts

Objective: To investigate changes of Ca2+ activated potassium channels (KCa) in autogenous vein grafts. Methods: Contraction of venous ring was measured by means of perfusion in vitro. The intimal rabbits proliferation of vascular and proliferation of cultured smooth muscle cells(vascular smooth muscle cells, VSMCs)were observed by the means of computerised image analysis and MTT method respectively. Furthermore, whole cell mode of patch clamp was used to record KCa of VSMCs isolated from autogenous vein grafts. Results: One week after transplantation there were no significant differences of contraction and intimal relative thickness between autogenous vein grafts and control. Contraction and intimal relative thickness of autogenous vein graft were significantly increased 2 weeks after transplantation (P<0.05, n=8 vs control), and they was more enhanced 4 weeks after vein transplantation (P<0.01, n=8 vs control).TEA(blocker of Ca2+ activated potassium channels)increased MTT A490 nm value of VSMCs from femoral vein in a dose dependent manner(P<0.05, n=8). KCa current density was significantly attenuated in VSMCs from autogenous vein grafts (1-4) week after transplantation(P<0.05, n=5).Conclusion: KCa is inhibited in autogenous vein graft, which account for vasospasm and intimal proliferation.

Inhibition of angiogenesis by DADAG in vivo and in vitro

1,2,5,6-Dianhydro-3,4-diacetyl-galactitol （DADAG）, an alkylating sugar alcohol derivative, has been shown effective against tumor growth. In this research, we explored the effect of DADAG on angiogenesis in chick chorioallantoic membrane （CAM） model and on the proliferation and migration of human umbilical vein endothelial cells （HUVECs）. We also studied the possible mechanism of the anti-angiogenesis effect of DADAG. The results showed that DADAG （100, 500 and 1000μnol/L） inhibited angiogenesis in CAM model dose-dependently. Sulforhodamine B （SRB） assay indicated that DADAG （45, 90, 135, 180 and 225 μmol/L） suppressed HUVECs proliferation in a dose-dependent and time-dependent manner. High Content Screening （HCS, Cellomics） assay, in which the influence of cell proliferation on migration could be excluded, indicated that DADAG （45, 135 and 225 ~xmol/L） directly inhibited the motility ofHUVECs. Immunofiuorescence assay suggested that DADAG inhibited angiogenesis possibly by decreasing vascular endothelial growth factor （VEGF） expression in HUVECs. Our findings reveal that DADAG show anti-angiogenic activity in vivo and in vitro, which is related to the downregulation of VEGF expression in endothelial cells.

Regulation of tissue repair and regeneration by electric fields

Endogenous electric fields （EFs） have been detected at wounds and damaged tissues. The potential roles of EFs in tissue repair and regeneration have been an intriguing topic for centuries. Recent researches have provided significant insights into how naturally occurring EFs may participate in the control of tissue repair and regeneration. Applied EFs equivalent to the size of fields measured in vivo direct cell migration, cell proliferation and nerve sprouting at wounds. More remarkably, physiological EFs are a guidance cue that directs cell migration which overrides other well accepted directional signals including initial injury stimulation, wound void, contact inhibition release, population pressure and chemotaxis. EFs activate many intracellular signaling pathways in a directional manner. Modulation of endogenous wound EFs affects epithelial cell migration, cell proliferation, and nerve growth at cornea wounds in vivo. Electric stimulation is being tested clinically for the treatments of bone fracture, wound healing and spinal cord injury. EFs thus may represent a novel type of signaling paradigm in tissue repair and regeneration. Combination of the electric stimulation and other well understood biochemical regulatory mechanisms may offer powerful and effective therapies for tissue repair and regeneration. This review introduces experimental evidence for the existence of endogenous EFs and discusses their roles in tissue repair and regeneration.

Curcumin-encapsulated polymeric nanoparticles for metastatic osteosarcoma cells treatment

Osteosarcoma is a high-class malignant bone cancer with a less than 20% five-year survival rate due to its early metastasis potential. There is an urgent need to develop a versatile and innoxious drug to treat metastatic osteosarcoma.Curcumin（Cur） has shown its potential for the treatment of many cancers; however,the clinical implication of native curcumin is severely hindered by its intrinsic property. In this study,a mixed system of monomethoxy（polyethylene glycol）-poly（d,l-lactide-co-glycolide）/poly（ε-caprolactone）（m PEGPLGA/PCL） was used to build a formulation of curcuminencapsulated nanoparticles（Cur-NPs）,which significantly improved the solubility,stability and cellular uptake of curcumin. Moreover,the Cur-NPs were superior to free curcumin in the matter of inhibition on the proliferation,migration and invasion of osteosarcoma 143B cells. It was found that both free curcumin and Cur-NPs could decrease the expressions of c-Myc and MMP7 in the level of mRNA and protein,which explained why free curcumin and Cur-NPs could inhibit the proliferation and invasion of metastatic osteosarcoma 143B cells. The Cur-NPs provided a promising strategy for metastatic osteosarcoma treatment.