Exploring the effects of naringin on oxidative stress-impaired osteogenic differentiation via the Wnt/ß-catenin and PI3K/Akt pathways.

This study aimed to explore naringin's potential to promote the osteogenic differentiation of MC3T3-E1 under oxidative stress. It delved into Nar's connection with the Wnt/ß-catenin and PI3K/Akt signaling pathways. Initially, 2911 OP-related genes were analyzed, revealing close ties with the PI3K/Akt and Wnt pathways alongside oxidative stress. Nar's potential targets-ESR1, HSP90AA1, and ESR2-were identified through various databases and molecular docking studies confirmed Nar's affinity with ESR1 and HSP90AA1. Experiments established optimal concentrations for Nar and H2O2. H2O2 at 0.3 mmol/L damaged MC3T3-E1 cells, alleviated by 0.1 µmol/L Nar. Successful establishment of oxidative stress models was confirmed by DCFH-DA probe and NO detection. Nar exhibited the ability to enhance osteogenic differentiation, counteracting oxidative damage. It notably increased osteoblast-related protein expression in MC3T3-E1 cells under oxidative stress. The study found Nar's positive influence on GSK-3ß phosphorylation, ß-catenin accumulation, and pathway-related protein expression, all critical in promoting osteogenic differentiation. The research concluded that Nar effectively promotes osteogenic differentiation in MC3T3-E1 cells under oxidative stress. It achieved this by activating the Wnt/ß-catenin and PI3K/Akt pathways, facilitating GSK-3ß phosphorylation, and enhancing ß-catenin accumulation, pivotal in osteogenesis.

N-Type Small Molecule Electron Transport Layers with Excellent Surface Energy and Moisture Resistance Siloxane for Non-Fullerene Organic Solar Cells.

Electron transport layers (ETLs) generally contain polar groups for enhancing performance and reducing the work function. Nevertheless, the polar group with high surface energy may cause inferior interfacial compatibility, which challenges the ETLs to balance stability and performance. Here, two conjugated small molecules of ETLs with low surface energy siloxane, namely PDI-Si and PDIN-Si, are synthesized. The siloxane with low surface energy not only enhances the interfacial compatibility between ETLs and active layers but also improves the moisture-proof stability of the device. Impressively, the amine-functionalized PDIN-Si can simultaneously exhibit conspicuous n-type self-doping properties and outstanding moisture-proof stability. The optimization of interfacial contact and morphology enables the PM6:Y6-based OSC with PDIN-Si to achieve a power conversion efficiency (PCE) of 15.87%, which is slightly superior to that of classical ETL PDINO devices (15.27%), and when the PDIN-Si film thickness reaches 28 nm, the PCE remains at 13.19% (≈83%), which indicates that PDIN-Si has satisfactory thickness insensitivity to facilitate roll-to-roll processing. Excitingly, after 120 h of storage in an environment with humidity above 45%, the unencapsulated device with PDIN-Si as ETL remains at 75% of the initial PCE value, while the device with PDINO as ETL is only 50%.

Naringin Alleviates H2O2-Inhibited Osteogenic Differentiation of Human Adipose-Derived Stromal Cells via Wnt/ß-Catenin Signaling.

Osteoporosis is an age-related systemic bone disease that places a heavy burden on patients and society. In this study, we aimed to investigate the effects of naringin (NAR) on the osteogenic differentiation of human adipose-derived stromal cells (ADSCs). The results demonstrated that NAR pretreatment effectively abated H2O2-induced cell death and ROS accumulation in ADSCs undergoing osteogenic differentiation (ADSCs-OD). In addition, we also observed that the impaired extracellular matrix mineralization and ALP activity in H2O2-stimulated ADSCs-OD were notably rescued by NAR pretreatment. Moreover, the effects of H2O2 exposure on Wnt/ß-catenin signaling in ADSCs-OD were largely reversed by NAR pretreatment. Collectively, our findings indicated that NAR could protect ADSCs-OD against H2O2-inhibited osteogenic differentiation.

Patient education by smartphones for bowel preparation before colonoscopy.

BACKGROUND AND AIM: We aim to evaluate the effect of smartphone education on the bowel preparation quality of patients undergoing colonoscopy by meta-analysis. METHODS: Randomized controlled trials using smartphones to educate patients on bowel preparation for colonoscopy were screened from the PubMed, Web of Science, Cochrane Library, and Embase databases from inception to August 31, 2021. After extracting the data, Review Manager software was used for meta-analysis. RESULTS: A total of 12 randomized controlled trials with 4165 patients were included in the meta-analysis. There were 2060 patients in the smartphone group, including 1784 patients with adequate bowel preparation, with a rate of 86.6%, and 2105 patients in the control group, including 1614 patients with adequate bowel preparation, with a rate of 76.7%, and pooled risk ratio (RR) was 1.15 (95% confidence interval [CI]: 1.07-1.23, P < 0.01). Eight included studies reported the adenoma detection rate. The adenoma detection rate in the smartphone group was 26.2%, and the rate in the control group was 19.3%, with an RR of 1.29 (95% CI: 1.03-1.62, P < 0.05). CONCLUSION: Using smartphones to educate patients on bowel preparation for colonoscopy improved the quality of bowel preparation and increased the adenoma detection rate.

MicroRNA-365-3p inhibits bone marrow mesenchymal stem cell differentiation into islet-like cell clusters via targeting Pax6 and inhibiting the MEK/ERK pathway.

BACKGROUND: Diabetes has severe impacts on the health of patients. The differentiation of mesenchymal stem cells (MSCs) into islet-like cell clusters (ICCs) is an effective protocol for the treatment of diabetes. microRNAs (miRs) regulate multiple cellular processes including cell differentiation. This study sought to identify the mechanism of miR-365-3p in the differentiation of bone marrow MSCs (bMSCs) into ICCs. METHODS: Initially, the differentiation of bMSCs into ICCs was induced. Then, the miR-365-3p expression pattern in the bMSCs and ICCs was detected. Next, the miR-365-3p expression pattern was silenced in bMSCs to assess the effect on differentiation efficiency and measure the expressions of ICC marker genes during the differentiation of bMSCs into ICCs. The miR-365-3p downstream target genes were predicted and verified. Paired box protein 6 (Pax6) was downregulated in bMSCs with silenced miR-365-3p to evaluate the differentiation of bMSCs into ICCs. Furthermore, the Pax6 downstream pathway was evaluated. RESULTS: The differentiation of bMSCs into ICCs was successfully induced. The miR-365-3p expression in bMSCs was higher than that in ICCs. miR-365-3p downregulation in bMSCs facilitated the differentiation of bMSCs into ICCs, as evidenced by elevated releases of insulin and C-peptide in ICCs and elevated expressions of ICC marker genes. Our findings denoted that miR-365-3p targeted Pax6. Inhibition of Pax6 expression annulled the promotion of miR-365-3p downregulation on the differentiation of bMSCs into ICCs. Increased phosphorylation levels of MEK and ERK were identified in ICCs after downregulation of miR-365-3p however they were decreased after downregulation of Pax6. CONCLUSIONS: This study supported that miR-365-3p inhibited the differentiation of bMSCs into ICCs via targeting Pax6 and inhibiting the MEK/ERK pathway.

Construction of a risk map to understand the vulnerability of various types of cancer patients to COVID-19 infection.

COVID-19 is leading to a global pandemic and invades human cells via ACE2. ACE2 was found to be abundantly expressed in many organs and cells. However, there is no evidence about the potential risk of various types of cancer patients vulnerable to the infection of COVID-19. To obtain a risk map that indicates the novel coronavirus vulnerability of different types of cancer, we analyzed in this work the RNA sequencing datasets of cancer patients. By interrogating the datasets, we not only identified the cancer types vulnerable to COVID-19 attacks, but also we reported that variations in the mRNA expression level of ACE2 correlate to various prognosis phenomenon in different types of cancer cohorts, and illustrated the underlying mechanism involved or may be related to lymphocytes infiltration. From these discoveries, we constructed an infection risk map, which indicates the vulnerability of different types of cancer to COVID-19 infection, also elucidated the correlationship between ACE2 and the prognosis of cancer. We found that high ACE2 expression levels lead to high risk of COVID-19 infection and poor prognosis of breast invasive carcinoma (BRCA), while better prognosis in ovarian serous cystadenocarcinoma (OV) patient cohorts. Moreover, our study demonstrated that this different pattern may correlate with the immune infiltration level.

miR-193a/b-3p relieves hepatic fibrosis and restrains proliferation and activation of hepatic stellate cells.

MicroRNAs (miRNAs) have been confirmed to participate in liver fibrosis progression and activation of hepatic stellate cells (HSCs). In this study, the role of miR-193a/b-3p in concanavalin A (ConA)-induced liver fibrosis in mice was evaluated. According to the results, the expression of miR-193a/b-3p was down-regulated in liver tissues after exposure to ConA. Lentivirus-mediated overexpression of miR-193a/b-3p reduced ConA-induced liver injury as demonstrated by decreasing ALT and AST levels. Moreover, ConA-induced liver fibrosis was restrained by the up-regulation of miR-193a/b-3 through inhibiting collagen deposition, decreasing desmin and proliferating cell nuclear antigen (PCNA) expression and lessening the content of hydroxyproline, transforming growth factor-ß1 (TGF-ß1) and activin A in liver tissues. Furthermore, miR-193a/b-3p mimics suppressed the proliferation of human HSCs LX-2 via inducing the apoptosis of LX-2 cells and lowering the levels of cell cycle-related proteins Cyclin D1, Cyclin E1, p-Rb and CAPRIN1. Finally, TGF-ß1 and activin A-mediated activation of LX-2 cells was reversed by miR-193a/b-3p mimics via repressing COL1A1 and α-SMA expression, and restraining the activation of TGF-ß/Smad2/3 signalling pathway. CAPRIN1 and TGF-ß2 were demonstrated to be the direct target genes of miR-193a/b-3p. We conclude that miR-193a/b-3p overexpression attenuates liver fibrosis through suppressing the proliferation and activation of HSCs. Our data suggest that miR-193a-3p and miR-193b-3p may be new therapeutic targets for liver fibrosis.

OCIAD2 suppressed tumor growth and invasion via AKT pathway in Hepatocelluar carcinoma.

Hepatocellular carcinoma (HCC) is an aggressive tumor and the third leading cause of cancer-related death worldwide. Ovarian carcinoma immunoreactive antigen-like protein 2 (OCIAD2) has been found frequently methylated in various cancers, including HCC. The aim of the present study was to investigate the role of OCIAD2 in HCC progression. We analyzed liver hepatocellular carcinoma patients' data from the Cancer Genome Atlas (TCGA), including data extracted from 371 HCC tissues and 50 adjacent normal liver tissues. The RNA sequencing and DNA methylation data revealed that OCIAD2 were significantly hypermethylated and its expression level in the tumor tissues was much lower than that in the corresponding adjacent normal tissues. The methylation level in the promoter was negatively correlated with the expression level of OCAID2. Treatment of HCC cell lines with the DNA methylation inhibitor 5-aza-2'-deoxycitydine (5-Aza) induced a significant increase in the OCIAD2 mRNA and protein. Knocking-down OCIAD2 led to an increased colony formation, migration and invasion dramatically, accompanying with an enhanced expression of MMP9 and activation of AKT and FAK. Inhibition of AKT signaling restored OCIAD2-mediated changes in HCC cell clonogenic growth, migration and invasion. Survival analysis of HCC patient's data indicated patients with a higher expression ratio of OCIAD2/MMP9 had a shorter overall survival than those with a lower expression ratio of OCIAD2/MMP9. Overall, our data indicate that reduced expression of OCIAD2 by DNA hypermethylation plays an important role in HCC tumor growth and invasion. Hypermethylation of OCIAD2 may contribute to HCC treatment development.

[Fast measurement method based on near infrared spectroscopy in extraction process of Tianshu capsules].

Based on the near infrared spectroscopy, partial least square (PLS) method was used to respectively develop the quantitative calibration models to fast measure the contents of the total solid and ferulic acid in extraction process of Tianshu capsule extracts. The results showed that in the quantitative model of solid content, the correlation coefficients (R²) of calibration set and cross validation set were 0.967 301 and 0.947 726. The root-mean square error of calibration set (RMSEC) was 0.054 7 and root-mean square error of cross validation set (RMSECV) was 0.069 8. Besides, in the quantitative model of ferulic acid, the correlation coefficients (R²) of calibration set and cross validation set were 0.986 879 and 0.962 243. RMSEC was 1.402 6 and RMSECV was 2.400 2. When the established models were applied to on-line monitoring, the correlation coefficients of predicted results and measured values for total solid content and ferulic acid were 0.993 3 and 0.991 6; root-mean square error of predicted value (RMSEP) was 0.039 3 and 1.669 3 respectively; mean relative deviation of predicted value (RSEP) was 3.49% and 3.58%. The results indicated that the established models can be used to fast measure the contents of the total solid and ferulic acid in extraction process of Tianshu capsule extracts.

[Impurity removal technology of Tongan injection in liquid preparation process].

In order to effectively remove the invalid impurities in Tongan injection, optimize the optimal parameters of the impurity removal technology of liquid mixing process, in this paper, taking Tongan injection as the research object, with the contents of celandine alkali, and sinomenine, solids reduction efficiency, and related substances inspection as the evaluation indexes, the removal of impurities and related substances by the combined process of refrigeration, coction and activated carbon adsorption were investigated, the feasibility of the impurity removal method was definited and the process parameters were optimized. The optimized process parameters were as follows: refrigerated for 36 h, boiled for 15 min, activated carbon dosage of 0.3%, temperature 100 degrees C, adsorption time 10 min. It can effectively remove the tannin, and other impurities, thus ensure the quality and safety of products.

[Optimization of one-step pelletization technology of Jiuwei Xifeng granules by response surface methodology].

Using the qualified rates of particles as the evaluation indexes, the impact tactors of one-step pelletization technology of Jiuwei Xifeng granules were selected from six factors by the Plackett-Burman experimental design and the levels of non-significant factors were identified. According to the Plackett-Burman experimental design, choosing the qualified rates of particles and angle of repose as the evaluation indexes, three levels of the three factors were selected by Box-Behnken of central composite design to optimize the experimental. The best conditions were as follows: the fluid extract was sprayed with frequency of 29 r . min-1, inlet air temperature was 90 °C, the frequency of fan was 34 Hz. Under the response surface methodology optimized scheme, the average experimental results are similar to the predicted values, and surface methodology could be used in the optimization of one-step pelletization for Chinese materia medica.

[Effect of platelet rich plasma on the proliferation behavior of human MG63 osteoblast-like cells in vitro].

OBJECTIVE: To assess the effect of platelet rich plasma (PRP) on proliferation and differentiation of human MG63 osteoblast-like cells and the biological function of PRP in vitro. METHODS: PRP was obtained from venous blood of a health volunteer by two step centrifugation. CaCl2 and thrombin were used to activate PRP. The differentiation of MG63 cells, which were exposed to various concentrations of PRP (0, 1%, 2%, 3%) was detected by alkaline phosphatase (ALP) activity. Propidium iodide (PI) fluorescent coloration staining was used to observe the morphology of cells. Immunocytochemistry was used to evaluate the expression level of transforming growth factor-beta (TGF-beta) in MG63 cells in different concentration of PRP. The cells adhered to calcium phosphate material was observed by scanning electron microscopy (SEM). The proliferation was evaluated by cell counting kit-8 (CCK-8) proliferation assay. The cell cycle assay was performed by low cytometry (FCM) to detect the effect of PRP on MG63 cells in different time points. The mRNA level of Col-I in MG63 cells cultured under different concentration PRP was checked by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: ALP activity experiment demonstrated that the maximum effect was got in 3% PRP group. PRP had a positive effect on the proliferation of MG63 cells but cells also presented disengage phenomena from the glass slides. The PI staining showed that PRP improved fluorescent intensity of cell nucleus. Immunocytochemistry showed that TGF-beta expression level was significantly enhanced on 3% PRP group (P<0.05). SEM showed that cells grew well on material in PRP group. The results of CCK-8 showed that the mean absorbency number A(450 nm) of 4.8% PRP was significantly higher than that of control group (P<0.05). FCM showed that S period cells percentage of PRP group was higher than that of control group in the 2nd day (P<0.05); G0/G1 period cells percentage of PRP group was significant increased than that of control group in the 10th day (P<0.05); G2/M period cells percentage of PRP group was higher than that of control group except the 6th day. PRP promoted the expression of Col- I in MG63 cells by RT-PCR. CONCLUSION: These data suggest that PRP has a positive influence on MG63 proliferation, transference and the expression of relative protein and gene in an appropriated concentration. The findings of this study also demonstrated that PRP may play a beneficial role of unifying and modulating the biological behavior of MG63 cells.

The feedback regulation of PI3K-miR-19a, and MAPK-miR-23b/27b in endothelial cells under shear stress.

Mechanical stimulation regulates endothelial cell (EC) functions through the modulation of signaling networks and gene expression. Our recent studies have identified that shear stress regulation of microRNAs (miRs)-19a, 23b and 27b, led to the modulation of EC proliferation. However, the underlying molecular mechanisms by which shear stress regulates these miRs have not been explored. Previous studies showed that shear stress activates multiple signaling pathways, including phosphatidylinositol 3 kinase (PI3K) and mitogen-activated protein kinase (MAPK). In this work we demonstrate that inhibition of the PI3K pathway attenuated the shear-induced miR-19a, and inhibition of the MAPK pathway attenuated miR-23b, 27b. The knockdown of miR-19a using antagomir-19a oligonucleotide (AM19a) decreased the shear-induced PI3K activation; whereas AM-23b, 27b reduced the shear-induced MAPK activation. Furthermore, the overexpression of miR-19a overrode the suppressive effects of PI3K inhibitors on shear-induced PI3K activation; the overexpression of miR-23b, 27b had similar effects on ERK activations, but had little effect on P38 and JNK activation. Our findings suggest a positive feedback loop whereby PI3K and MAPK mediate the shear regulation of miR expression, which in turn modulates the shear-regulated PI3K/MAPK signaling events in ECs.

[Constructing a phage-displayed random mutation library of HIV-1 Tat38-61 at the sites of 51 and 55 amino acids in basic region].

We constructed a phage-displayed random mutation library of Tat38-61(51N/55N), for studying the molecular evolution screening of HIV-1 Tat38-61 epitope. We used primers containing the random nucleotide sequences, and introduced the random mutations at the sites of 51 and 55 amino acids coding sequences into full-length Tat sequences by overlapping PCR. With the randomly mutated full-length Tat as template, the Tat38-61(51N/55N) mutants which contained recognition sequences for the Xba I in both ends were amplified by PCR using the designed primers. The mutants were cloned into Xba I site in the phagemid vector pCANTAB5S, then the recombinants were transformed into E. coli TG1, a phage-displayed the random mutation library of Tat38-61(51N/55N) was constructed by the rescue of help virus M13KO7. The results showed that the library consisted of about 5.0 x 10(6) colonies and the phage library titer was 2.65 x 10(12) TU/mL. More than 56.50% colonies in the library were positive for insertion. Sequence analysis showed that the nucleotides encoding amino acids at the sites of 51 and 55 distributed randomly. The constructed mutation library could meet the requirements for the following molecular evolution screening, and might prepare the Tat mutants for the further study of new Tat vaccine candidates.

High efficient isolation and systematic identification of human adipose-derived mesenchymal stem cells.

BACKGROUND: Developing efficient methods to isolate and identify human adipose-derived mesenchymal stem cells (hADSCs) remains to be one of the major challenges in tissue engineering. METHODS: We demonstrate here a method by isolating hADSCs from abdominal subcutaneous adipose tissue harvested during caesarian section. The hADSCs were isolated from human adipose tissue by collagenase digestion and adherence to flasks. RESULTS: The yield reached around 1 × 10(6) hADSCs per gram adipose tissue. The following comprehensive identification and characterization illustrated pronounced features of mesenchymal stem cells (MSCs). The fibroblast-like hADSCs exhibited typical ultrastructure details for vigorous cell activities. Karyotype mapping showed normal human chromosome. With unique immunophenotypes they were positive for CD29, CD44, CD73, CD105 and CD166, but negative for CD31, CD34, CD45 and HLA-DR. The growth curve and cell cycle analysis revealed high capability for self-renewal and proliferation. Moreover, these cells could be functionally induced into adipocytes, osteoblasts, and endothelial cells in the presence of appropriate conditioned media. CONCLUSION: The data presented here suggest that we have developed high efficient isolation and cultivation methods with a systematic strategy for identification and characterization of hADSCs. These techniques will be able to provide safe and stable seeding cells for research and clinical application.

[Morphological characteristics of human adipose-derived stem cells].

This paper is aimed to isolate and to cultivate human adipose-derived stem cells (hADSCs) from the adipose tissue by a combination of collagenase digestion, adherence to flasks and monoclonal cultural method so as to observe the morphological characteristics of the hADSCs. The immunophenotypes of hADSCs were detected by flow cytometry techniques. The general morphological characteristics of hADSCs were observed by cytochemical and immunofluorescent techniques. The ultrastructure of hADSCs was observed by transmission electron microscopy (TEM). The experimental results showed that hADSCs had unique immunophenotypes and they were positive for CD29, CD44, CD90, CD105 and CD166, but negative for CD31, CD45 and HLA-DR. Cytochemistry showed that cytoplasm of hADSCs was stained with light blue by hematoxylin-eosin, negative for Oil red O and AKP, and positive for immunofluorescence CD29 and CD166. There were abundant organella and microvilli in the ultrastructure of hADSCs. The results validate that they will offer a morphological foundation for application of the hADSCs.

[Directional differentiation of human adipose-derived stem cells into endothelial cells].

OBJECTIVE: To investigate the possibility of directional differentiation of human adipose stem cells (hADSCs) into endothelial cells (EC), so as to provide seed cells for tissue engineered vessels. METHODS: hADSCs were isolated from human adipose tissue by collagenase digestion, cultured and amplified by adherence to flasks. Then hADSCs were directionally induced to differentiate into EC by a combination of fibronectin (FN), endothelial cells support liquid (EGM2-MV) containing various growth factors and high concentration of VEGF165 (50 ng/ml). Then, the cells morphology, phenotype and function were identified. RESULTS: Highly homologous hADSCs were obtained, and then hADSCs were directionally differentiated into EC. CD31 and CD34, the specific markers for EC, and vascular endothelial growth factor receptor (KDR) were positive by immunohistochemical staining and RT-PCR. In addition, unique Weibel-Palade bodies in EC were observed under transmission electron microscope. Functionally, hADSCs could swallow Dil-Ac-LDL and form tube-like structures in matrigel after endothelial differentiation. CONCLUSIONS: hADSCs can be successfully induced to differentiate into endothelial cells in vitro.

Novel evolved immunoglobulin (Ig)-binding molecules enhance the detection of IgM against hepatitis C virus.

Detection of specific antibodies against hepatitis C virus (HCV) is the most widely available test for viral diagnosis and monitoring of HCV infections. However, narrowing the serologic window of anti-HCV detection by enhancing anti-HCV IgM detection has remained to be a problem. Herein, we used LD5, a novel evolved immunoglobulin-binding molecule (NEIBM) with a high affinity for IgM, to develop a new anti-HCV enzyme-linked immunosorbent assay (ELISA) using horseradish peroxidase-labeled LD5 (HRP-LD5) as the conjugated enzyme complex. The HRP-LD5 assay showed detection efficacy that is comparable with two kinds of domestic diagnostic kits and the Abbott 3.0 kit when tested against the national reference panel. Moreover, the HRP-LD5 assay showed a higher detection rate (55.9%, 95% confidence intervals (95% CI) 0.489, 0.629) than that of a domestic diagnostic ELISA kit (Chang Zheng) (53.3%, 95% CI 0.463, 0.603) in 195 hemodialysis patient serum samples. Five serum samples that were positive using the HRP-LD5 assay and negative with the conventional anti-HCV diagnostic ELISA kits were all positive for HCV RNA, and 4 of them had detectable antibodies when tested with the established anti-HCV IgM assay. An IgM confirmation study revealed the IgM reaction nature of these five serum samples. These results demonstrate that HRP-LD5 improved anti-HCV detection by enhancing the detection of anti-HCV IgM, which may have potential value for the early diagnosis and screening of hepatitis C and other infectious diseases.

[Effect of bone marrow mesenchymal stem cells on tumor neovascularization].

OBJECTIVE: The effect of human bone marrow mesenchymal stem cells (hMSCs) on tumor neovascularization were studied. METHODS: hMSCs were isolated from human bone marrow by density gradient fractionation and adherence to plastic flasks. hMSCs-EGFP were obtained by pLEGFP-N1 retroviral vector. Flow cytometry was used to detect the cell surface antigen and the differentiation potential of hMSCs-EGFP was investigated under conditioned media. The effect of hMSCs on tumor neovascularization were observed by establishing solid tumor models in BALB/C nude mice. In addition, effect of the conditioned medium used for tumor cells and endothelial cells (EC) cultivation was collected, to detect its effect on the growth and migration rates of hMSC. hMSCs were induced to differentiate into EC in vitro and the migratory effect on HUVEC was also evaluated. RESULTS: hMSCs-EGFP, like hMSC, exhibited a fibroblast-like morphological feature, and both had the similar cell surface antigens. They could be induced into osteocytes or adipocytes under the conditioned media. The results not only suggested that hMSCs contributed to tumor neovascularization, but also indicated that most of vessels were host-derived angiogenesis mediated by hMSCs. The mean vascular density (MVD) in suspension group (13.67 ± 1.53) was strikely higher than that in MCF-7 group (5.33 ± 1.42), which showed statistical significance (P < 0.05). Only very few vessels were attributed to hMSCs transdifferentiation into ECs. Tumor cells and ECs can promote hMSCs proliferation and migration through paracrine action. Furthermore, hMSCs were positive for CD31 after 2 weeks induction and HUVEC migration can be facilitated by hMSCs. CONCLUSION: MSCs have the effect of promoting tumor neovascularization.