To explore the effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the growth of human lung cancer cell lines and its possible mechanism.

To investigate the effects of glycyrrhizin on genes expression during the process of rat liver fibrosis.

To investigate the effects of cyclosporin A on insulin release and the gene expression profiles of mitochondrial oxidative phosphorylation in NIT-1 cells.

Overexpression of lung resistance-related protein(LRP) is involved in multidrug resistance and poor outcome in acute leukemia. This study was designed to investigate the effect of sodium butyrate (NaB) on LRP expression level and the function of LRP in K562 cells.

To quantitatively evaluate the effects of BMP-2 on the COMP gene expression in both primary human chondrocytes and chondrogenic cell line ATDC55.

To study effect of downregulation of c-myc gene expression with As2O3 on inducing Ec109 cell apoptosis.

To study the influence of adjustment of balance of Th1/Th2 by external cytokines on proliferation of glioma cells.

To study the co-localization of glucocorticoid receptor and 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) and to investigate whether glucocorticoids regulate the reductase activity and expression of 11beta-HSD1.

To investigate the effect of thalidomide on bone marrow cells gene expression in multiple myeloma (MM) patients with suppression subtractive hybridization (SSH) and explore the molecular mechanism of thalidomide therapy for MM.

To explore the effect of T(3) on the expression of transferrin receptor (TfR) and ferritin (Fn) in K562 cells and its possible mechanism.

To investigate the effect of arsenic trioxide (As(2)O(3)) on vascular endothelial growth factor (VEGF) expression in different courses of chronic myeloid leukemia (CML), VEGF level was measured with ELISA in the cultural supernatants of bone marrow mononuclear cells from CML patients. The results showed that supernatants of cultured bone marrow cells from 35 CML patients (20 chronic, 8 accelerated and 7 blast crisis phases) contained significantly higher VEGF levels (649.16 +/- 382.20 pg/ml, 560.27 +/- 409.14 pg/ml and 587.18 +/- 415.28 pg/ml, respectively) than that in 15 normal control samples (152.16 +/- 150.09 pg/ml; P < 0.01), but no significant differences were found in VEGF levels among different phases of CML. The bone marrow cells treated with As(2)O(3) (5 x 10(-6)mol/L) for 72 hours resulted in significant reduction of VEGF levels (down to 396.66 +/- 257.47 pg/ml, 363.42 +/- 239.85 pg/ml and 407.47 +/- 219.38 pg/ml, respectively) (P < 0.05). In conclusion, abnormal high expression of VEGF plays a role in the pathogenetic course of CML and it is probably an additional anticancer mechanism for As(2)O(3) to inhibit VEGF expression of leukemic cells.

This study was designed to explore the influence of STI571, a tyrosine kinase inhibitor, on the expression of c-kit in the bone marrow cells from patients with acute non-lymphocytic leukemia (ANLL). The cells were exposed to various concentration of STI571 for 72 hours, the expression of c-kit mRNA and CD117 was assayed by RT-PCR and flow cytometry, respectively. The results showed that STI571 treatment induced concentration-dependent decrease of c-kit and CD117 expression, which was significant lower than that in group before treatment and untreated control groups (P < 0.05) and 0.1 micro mol/L STI571 group was significantly higher than that in 10 micro mol/L group (P < 0.05). It is concluded that STI571 has an obvious effect on the restraint of c-kit in ANLL cells.

To investigate the correlation between matrix metalloproteinase 9 (MMP-9) expression and tumor invasion and metastasis as well, and to explore the potential application of controlled expression of target gene in tumor gene therapy.

To study the expression levels of ERCC2, UDG, and PCNA in cisplatin-treated A549 cell line.

To determine whether interferon-gamma (IFN-gamma)inhibit the expression of vascular endothelial growth factor (VEGF) in ovarian cancer cell line SKOV3 with the level of mRNA and protein.

HDL receptor plays a very important role in reverse cholesterol transport, and it represents a novel therapeutic target for atherosclerosis. For construction of an in vitro high-throughput drug screening model based on competitive receptor--ligand binding, the extracellular domain of HDL receptor was expressed in the methylotropic yeast Pichia pastoris. The DNA fragment encoding for extracellular domain of HDL receptor was cloned by RT-PCR from Hepatoma Bel-7402 total RNA and the nucleotide sequence of the cloned cDNA was verified by inserting it into pGEM-T vector. Then the cDNA was subcloned into pPIC9K, the integrative secretory expression plasmid of Pichia pastoris was constructed, with the methanol-inducible alcohol oxidase promoter and alpha-signal peptide. The recombinant plasmid was transformed into Pichia pastoris GS115 (His- strain) by electroporation. PCR was used to confirm the insertion of HDLR gene into the genome of Mut+ transformants. During cultivation the recombinant strain was induced by 1% methanol and supernatant was analyzed by SDS-PAGE and Western blot. The result showed a specific protein band at approximately 64.5 kDa after 5 days of induction. Then the ligand binding activity was confirmed using the DiI-AcLDL as ligand.

Streptomyces are Gram-positive, filamentous soil bacteria, which produce a wide variety of metabolites that are currently being exploited in both medicine and agriculture. Moreover, Streptomyces lividans is used as a host strain to effectively express and secrete heterologous proteins to culture media. Genes encoding Sec proteins responsible for the translocation of preproteins have been identified in S. lividans. SecYEG, a complex of integral membrane proteins SecY, SecE, and SecG in the cytoplasmic membrane, constitutes a pathway for polypeptide movement. SecA plays a central role in translocation as it is the site of preprotein entry into the translocase and it is the only ATPase essential for preprotein translocation. The role of SecD and SecF is to regulate the movement of the translocating protein. A better understanding of their regulatory mechanism could help to develop S. lividans strains with hyper-secretory capacity. In this study, a reporter system was used to investigate the regulatory mechanism of secE promoter. Upstream sequence (496 bp) of secE of S. lividans TK24 was cloned and characterized in a promoter probe vector pIJ4083 upstream of promoterless xylE. Sequencing analysis revealed that secE upstream sequence of S. lividans shares 99.8% homology with the secE promoter of S. coelicolor. The transcriptive activity of this fragment approximates vsi promoter in CMI medium, a strong promoter from S. venezuelae. The activity of secE promoter was observed in different growth phase, culture temperature and culture media. The expression level of secE was higher during the log phase, but decreased at the beginning of the stationary phase. At growth temperature of 28 degrees C, the expression level was much higher than that at 37 degrees C. When the bacteria were incubated in NB, Phage, and CM medium respectively, the expression level of secE promoter was different at a certain fermentation time, but all reached the highest level at log phase. Further analysis revealed that glucose may repress secE promoter expression.

Gene amplification is a common mechanism that contributes to the drug resistance. To explore the molecular genetic background related to the MTX resistance in the mouse MTX-resistant cells, differential PCR was used to determine the amplification and overexpression of DHFR gene. In addition, the correlations between c-myc, p53 status and dhfr amplification were studied. Amplification and overexpression of dhfr suggested its role in MTX-resistant cells. However, no amplification and overexpression of c-myc were detected. On the other hand, no alteration of p53 copy number was found. The increased mRNA level of p53 suggested the normal function of p53. These results implicated the status of c-myc and p53 had no correlation with dhfr amplification, therefore some other molecular genetic alterations may exist to permit the dhfr amplification in MTX-resistant cells.

To investigate the expression of cyclins related gene in HL60 cells before and after arsenic trioxide treatment by gene chip.