OBJECTIVETo study the inhibitory effect of wogonin on the growth and proliferation of breast cancer cells MDA-MB-23, and observe its effect on the adhesion, migration and invasion of MDA-MB-23 cells, in order to further study its molecular mechanism.

METHODMTT assay was used to detect the effect of wogonin on MDA-MB-23 cell growth. Ki-67 assay was adopted to test the effect of wogonin on cell proliferation. Scratch test, adherence test and invasion chamber assay were taken to detect the effect on the migration and invasion abilities of MDA-MB-231 cells. Proliferation and metastasis-related proteins and relevant signaling pathways were detected by Western blotting.

RESULTWogonin could remarkably inhibit the growth and proliferation of MDA-MB-231 cells, significantly inhibit migration, adhesion and invasion abilities of breast cancer cells at a low concentration, and effectively inhibit the expression of Survivin, Bcl-2, ICAM-1, MMP-2, MMP-9 proteins of MDA-MB-231 cells.

CONCLUSIONWogonin could notably inhibit growth and proliferation of breast cancer cells, and inhibit migration, adhesion and invasion of MDA-MB-231 cells. Its invasive and adhesive effects on MDA-MB-231 cells may be related to the decrease in ICAM-1, MMP-2, MMP-9 expressions.

Breast Neoplasms ; genetics ; metabolism ; pathology ; physiopathology ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Female ; Flavanones ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Neoplasm Invasiveness ; Signal Transduction ; drug effects

Adult ; Aged ; Anthracosis ; blood ; Humans ; Leptin ; blood ; Male ; Middle Aged ; Resistin ; blood

Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Sleep Apnea, Obstructive ; surgery ; Treatment Outcome

As CD40 transduces activation signals involved in inflammatory and immune disorders, we explored the expression and response to CD40 engagement in human glioma cell lines in this study. The CD40 expression in BT-325 and U251 cells was flow cytometrically detected. The cells were incubated with srhCD40L for 72 h to assess its effects on cell growth in vitro. TNF-α expression was quantified by real-time PCR, and protein expression was analyzed by ELISA. The I-κb mRNA was detected by RT-PCR. I-κB expression decreased after stimulation with 1 μg/mL srhCD40L, but it was upregulated after the cells were pretreated with CD40 antibody. srhCD40L significantly inhibited the proliferation of the CD40+ human glioma cells. The stimulation of CD40+ glioma cells with soluble CD40L (CD154) up-regulated the expression of TNF-α at both mRNA and protein levels. We are led to conclude that CD40L/CD40 could inhibit human glioma cells through I-κb signaling pathway. Interferon-γ can augment CD40 expression and the inhibitory effect of CD40 ligand on cell growth in vitro. These results suggest that srhCD40L may benefit the therapy strategy of glioma.

Smad3 is a major transporter in the transforming growth factor β (TGF-β) signaling pathway.It is in charge of the transfer of TGF-β signal from the surface of the cell membrane into the nucleus.The TGF-β signal can be bound to the target gene in the nucleus and regulate its expression.Abnormalities in Smad3 expression level and functional status will lead to abnormal signal transduction,involving cell growth,proliferation,development,differentiation,migration,apoptosis and other basic life activities.This review focused on the differential expression of Smad3 in hepatocellular carcinoma (HCC)and the adjacent tissue.The character of Smad3 in HCC is outlined in three parts:Smad3 upstream signaling source,Smad3 self-assembly maturation and Smad3 downstream effects,which may provide a summary and reference for the follow-up study on Smad3.

Animals ; Gene Expression Profiling ; Mitochondria, Heart ; genetics ; metabolism ; Myocardial Reperfusion Injury ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Administration, Oral ; Adolescent ; Condylomata Acuminata ; drug therapy ; Cyclophosphamide ; administration & dosage ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Penile Diseases ; drug therapy ; Vulvar Diseases ; drug therapy

Objective To investigate whether recombinant human endostatin can create a time window of vascular normalization prior to vascular pruning to alleviate hypoxia in Lewis lung carcinoma in mice. Methods Kinetic changes in morphology of tumor vasculature in response to recombinant human endostatin were detected under a confocal microscope with immunofluorescent staining in Lewis lung carcinomas in mice. The hypoxic cell fraction of different time was assessed with immunohistochemical staining . Effects on tumor growth were monitored as indicated in the growth curve of tumors . Results Compared with the control group vascularity of the tumors was reduced over time by recombinant human endostatin treatment and significantly regressed for 9 days. During the treatment, pericyte coverage increased at day 3, increased markedly at day 5, and fell again at day 7. The vascular basement membrane was thin and closely associated with endothelial cells after recombinant human endostatin treatment, but appeared thickened, loosely associated with endothelial cells in control tumors. The decrease in hypoxic cell fraction at day 5 after treatment was also found. Tumor growth was not accelerated 5 days after recombinant human endostatin treatment. Conclusions Recombinant human endostatin can normalize tumor vasculature within day 3 to 7, leading to improved tumor oxygenation. The results provide important experimental basis for combining recombinant human endostatin with radiation therapy in human tumors.

Objective To study the effect of the extract of Chrysanthemum Indicum(CI)on the expression of tumor necro-sis factor-α (TNF-α) and neutrophil function in chronic bronchitis (CB)rats and to explore the therapeutic mechanism for chronic bronchitis. Methods The extract of CI was prepared. Wistar rats were randomly divided into blank control group, model group, Chuanxiling group, and low-, middle-and high-dose CI extract groups. Rat model of CB was established by intratracheal injection with low-dose lipopolysaccharide. After drug intervention, the expression of TNF-α in rat serum and bronchoalveolar lavage fluid was detected by ELISA method. Phagocytic function of the neu-trophil and respiratory burst of the rats were measured by flow cytometry (FCM). Results Compared with the blank con-trol group, the phagocytic function of the neutrophil, respiratory burst of the rats, and the expression of TNF-α in rat serum and bronchoalveolar lavage fluid of the model group were increased significantly. CI extract significantly decreased the abnormal rising of the above indexes. Conclusion Down-Regulation of TNF-α expression, and decrease of the neutrophil phagocytic function and rat respiratory burst may be one of the therapeutic mechanisms of Chrysanthemum In-dicum extract for the treatment of CB.