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.

Antisense reconstruct, p16as E6E7Neo, harboring HPV-16E6E7 gene of which the expression is regulatable by dexamethasone was constructed. Calcium phosphate mediated transfection was employed to transduce this antisense reconstruct into HPV-16 positive CasKi cell line and HPV negative C-33A cell line (both derived from human cervical carcinoma) respectively. After dexamethasone was added into the culture medium to induce the expression of E6E7 antisense gene, the malignity of CasKi cells were reversed, while the growth characteristics and malignity of C-33A cells were unchanged. The results show that the reversing effect on CasKi cell is specific and mediated by inhibition of expression of E6E7 gene. It also demonstrated a more profound pathogenic role of HPV-16 E6E7 gene in the tumorogenesis of cervical carcinoma and provides a possibility for gene therapy of this tumor.

It has been well documented that the immune function declines with age in the human and animals. The possible causes for the decline are the inability of lymphocytes to proliferate in response to mitogenic stimulation and the decrease of IL-2 production. In the present studies, Rg1 was shown to selectively enhance the proliferation of lymphocytes and the production of IL-2 in aged rats. Using Northern blot and Western blot analyses, Rg1 was found to promote IL-2 gene expression which showed increase of IL-2 mRNA and IL-2 protein contents. Interestingly, under the same conditions, studies were carried out on the effect of Rg1 on the immune function of young adult rats, but no marked influence was observed. According to these results, it is reasonable to consider Rg1 an immunoregulator rather than a purely "immunopotentiating agent".

whiG gene has been subcloned into Streptomyces expression vector pAK203 containing inducible promoter tipA. The expression of whiG gene promoted the spore formation of S. coelicolor J1501 and recovered the sporulation ability of whiG-deficient S. coelicolor C71. Increased amount of whiG gene product was detected by Western blot hybridization after induction of thiostrepton. It will be helpful for the future study of in vitro transcription of whiG-dependent promoters.