To investigate the effect of laminin antisense RNA on laminin antisense RNA on the expression of E-cadherin, alpha-, beta-, gamma-catenins and focal adhesion kinase(FAK) stimulated by transforming growth factor beta(1)(TGFbeta(1)).

To explore the role of airway smooth muscle cells (ASMC) stimulated by inflammatory factors in the development of asthma and bronchial hyperresponsiveness (BHR) and the possible mechanism of low dose theophylline in the treatment of airway inflammation, the effects of GM-CSF on endothelin-1 and endothelin converting enzyme (ECE) gene expression in human ASMC and theophylline on their expressions were investigated.

To investigate whether nonenzymatic glycated end products (AGEs) have effects on the expression and bioactivity of plasminogen activator inhibitor-1 (PAI-1), one of the seripin proteinases, which lead to extracellular matrix (ECM) degradation in cultured human mesangial cells.

Angiotensinogen is the only known precursor of vasoactive angiotensin II and also one of the acute phase proteins. This study was intended to understand the regulation of angiotensinogen gene expression induced by IL-6.

To investigate the antitumor mechanism of interleukin-2 (IL-2) and interleukin-6 (IL-6) gene therapy.

To investigate the apoptosis of HL-60 cells induced by 9-cis retinoic acid (9-cis RA), and illustrate the possible molecular mechanism.

To define the prevalence of acquired red cell enzymopathy in leukemia and MDS patients and explore its clinical significance.

To evaluate whether the growth inhibition by retinoic acid and RAR alpha mRNA expression levels were affected by the change of ER expression.

To study the effect of IFN-alpha on the expressions of perforin and granzymes in IL-2-activated-lymphocytes.

To study the effects of mitogens on the expression of interleukin-2 receptor (IL-2R) and the cytotoxicity of human monocytes.

To investigate the effects of IFNs on the in vitro invasiveness and the expression of several genes related to invasion and metastatic behavior of MA-891 cells.

To study the biological significance of Grp94 deleted product (Grp94 beta) expressed in human colorectal carcinoma cells.

Human 17 beta-hydroxysteroid dehydrogenase type 1 (17 HSD type 1), encoded by HSD 17 B 1 gene, is a steroidogenic enzyme catalyzing the interconversion of estrone and estradiol. In this study, we investigated the role of cyclic adenosine 3', 5'-monophosphate (cAMP) in the regulation of 17 HSD type 1 expression in cultured choriocarcinoma cell lines. Treatment with 8-bromo-cAMP increased 17-HSD type 1 protein concentration in JAR and JEG-3 cells, and the induction was accompanied by parallel increase of 1.3 kb 17 HSD type 1 mRNA expression. Reporter gene analysis revealed that the activity of HSD 17 B 1 promoter in JAR and JEG-3 cells was induced by cAMP and that the region participating in transmission of cAMP effect is situated in the position between -659 and -550 in HSD 17 B 1 gene. The consequent electrophoretic mobility shift assay showed that this region formed specific DNA-protein complexes with nuclear extracts prepared from JAR, JEG-3, T-47 D and HeLa cells. The data provide the first evidence that HSD 17 B 1 gene transcription is activated by cAMP in choriocarcinoma cells.

To detect the activity of interleukin-6 (rhIL-6) on human lung cancer and the influences of recombinant human IL-6 (rhIL-6) on the in vitro growth of high-metastatic human lung giant cell carcinoma cell line PG and low-metastatic human lung adenocarcinoma cell line PAa.

To overcome the multidrug resistance (MDR) in tumor cells.

To explore the clinical implication of reversal of multidrug resistance (MDR) by cyclosporin A (CsA) in refractory and relapsed acute leukemias.

To illustrate the possible cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL).

MPS pulse therapy is quite effective for the treatment of lupus nephritis. At present, no research work has been reported on the relationship between MPS therapy and apoptosis and ICE expression in kidneys with lupus nephritis. We investigated the effects of MPS on the number of apoptotic cells and expression of ICE mRNA in the kidneys of fourmonth-old MRL-lpr/lpr mice, by means of image analysis system, RT-PCR and Northern blot. The results showed that in MPS group, the number of apoptotic cells in glomerular mesangium increased significantly, as compared with that of a control group (P < 0.05). Besides, the number of apoptotic cells in both the peri-tubule cells and peri-vascular infiltrating cells was also higher in MPS group than in the control group (both P < 0.01). Furthermore, higher expression of ICE mRNA was found in the treated group than in the control group. Our results suggest that MPS may induce both apoptosis and ICE mRNA expression in kidneys with nephritis, implying that apoptosis may be involved in the outcome of lupus nephritis treated with MPS.

Glucocorticoids have wide effects on the immune system, the mechanisms of these effects have not been clearly defined. The interaction of interleukin-2 (IL-2) with its receptor (IL-2R) is a critical control point in the T-cell mediated immune response. The effect of dexamethasone, a synthetic glucocorticoid hormone, on IL-2R is unclear in comparison with its inhibition on the accumulation of IL-2 mRNA. Our study shows that dexamethasone increases the basal and PHA-induced mRNA levels of IL-2R alpha gene in Jurkat cells, but it does not affect the expression of reporter gene constructs containing 5' flanking sequences (-482bp/ +16bp or -350bp/+16bp) of the IL-2R alpha gene in PHA activated Jurkat cells. These results indicate that dexamethasone plays a positive regulatory role in the IL-2R alpha gene expression, but the effect is not mediated by the previously identified proximal regulatory elements located between -482bp/+1bp. Meanwhile, our results also provide evidence that the activation mechanism of dexamethasone is different from that of PHA, and that dexamethasone and PHA show a synergistic effect in the induction of IL-2R alpha gene expression.

Using dot blot hybridization and flowcytometry, the effects of differentiation inducers retinoic acid (RA) and dimethyl sulfoxide (DMSO) on the resistant level of HL-60 cells and its resistant subline cells were studied. When the cells were treated with RA 1 mumol.L-1 for 24 h, the expression of MDR 1 mRNA evidently increased in both HL-60 and its multidrug resistant subline cells. The efflux of Rho-123 in the multidrug resistant subline cells was slightly decreased. But, when the cells were treated with 2% DMSO for 24 h the efflux of Rho-123 increased obviously. The results suggest that RA can induce the expression of MDR1 gene but perhaps inhibit the function of pump glycoprotein 170 (Pgp-170) through phosphorylation/dephosphorylation pathway. However, DMSO could induce the expression of full function of Pgp.