Biomedical subjects

Y Feng

Publications and source records attributed to Y Feng.

436 records · Page 25Linked to original sources

PubMedDate not supplied

Hypoxia-inducible factor 1alpha (HIF-1alpha) correlated with tumor growth and apoptosis in ovarian cancer.

The aims of this study were to investigate the hypoxia-inducible factor 1alpha (HIF-1alpha) protein inhibition and tumor growth by a molecular target of rapamycin inhibitor, rapamycin, in xenogeneic transplant model of ovarian cancer and to study the correlation of apoptosis with HIF-1alpha and vascular endothelial growth factor (VEGF) expression. Four groups of female nude mice were inoculated subcutaneous with SKOV-3 cells and treated with vehicle, rapamycin, paclitaxel, or rapamycin plus paclitaxel. The expressions of HIF-1alpha and VEGF and microvessel density (MVD) were assessed by immunohistochemistry. While messenger RNA (mRNA) expression of Glut1, bcl-2, and VEGF was studied by reverse transcription-polymerase chain reaction, and apoptosis of tumor cells was determined by terminal deoxynucleotidyl biotin-dUTP nick end labeling (TUNEL). The HIF-1alpha was expressed in epithelial ovarian cancer. There was a significant correlation between HIF-1alpha protein expression and VEGF or MVD. Tumor burden treated with rapamycin alone, rapamycin plus paclitaxel, and paclitaxel alone was reduced (47.91%, 51.03%, and 31.75%, respectively) compared with controls. The expression of HIF-1alpha was inhibited, and apoptotic index of tumor cell increased in rapamycin and rapamycin plus paclitaxel group. HIF-1alpha may upregulate VEGF expression both in mRNA and protein level. There is a positive correlation between HIF-1alpha and MVD. Rapamycin inhibits expression of HIF-1alpha and suppresses ovarian tumor growth. Our data suggested that a combination of HIF-1alpha inhibitor and chemotherapy could provide an effective approach for inhibiting tumor growth in ovarian cancer.

Actins↗

PubMedDate not supplied

Transcriptional profile of mechanically induced genes in human vascular smooth muscle cells.

Vascular smooth muscle cells must monitor and respond to their mechanical environment; however, the molecular response of these cells to mechanical stimuli remains incompletely defined. By applying a highly uniform biaxial cyclic strain to cultured cells, we used DNA microarray technology to describe the transcriptional profile of mechanically induced genes in human aortic smooth muscle cells. We first identified vascular endothelial growth factor (VEGF) as a mechanically induced gene in these cells; VEGF served as a positive control for these experiments. We then used a DNA microarray with 5000 genes with putative functions to identify additional mechanically induced genes. Surprisingly, relatively few genes are mechanically induced in human aortic smooth muscle cells. Only 3 transcripts of 5000 were induced >2.5-fold: cyclooxygenase-1, tenascin-C, and plasminogen activator inhibitor-1. Downregulated transcripts included matrix metalloproteinase-1 and thrombomodulin. The transcriptional profile of mechanically induced genes in human aortic smooth muscle cells suggests a response of defense against excessive deformation. These data also demonstrate that in addition to identifying large clusters of genes that respond to a given stimulus, DNA microarray technology may be used to identify a small subset of genes that comprise a highly specific molecular response.

Cells, Cultured↗

PubMedDate not supplied

Vascular dementia, with special reference to its vascular and immunological events.

Vascular dementia (VaD) is an poorly defined entity; it relates to different vascular mechanisms and different changes in the brain and has different clinical manifestations with different etiologies. From the pathogenetic and therapeutic point of view, we tried to find some practical events that could help identify VaD. We combined critical review with our own clinical and laboratory experience and found that some vascular, nonvascular, and immunological components are involved in the pathogenesis and treatment of VaD. We concluded that although the definition, etiology, clinical manifestation, laboratory data, and treatment are still controversial, it is useful to find some common, key points in the pathogenesis and treatment of VaD.

Dementia, Vascular↗

PubMedDate not supplied

Study on initiation of human lung carcinogenesis.

Cigarette smoking condensate and diethylnitrosamine can initiate human lung carcinogenesis as they are able to induce precancerous lesions of bronchioles and the transforming ability of human fetal lung (HFL) DNA. The induction of precancerous lesions in HFL and the acquirement of the transforming ability of HFL DNA by short-term exposure to carcinogens can be combined to yield an ideal model for the initiation of human lung carcinogenesis.

Animals↗