Biomedical subjects

Yi Huang

Publications and source records attributed to Yi Huang.

79 records · Page 5Linked to original sources

PubMed2002

IkappaB kinase activation is involved in regulation of paclitaxel-induced apoptosis in human tumor cell lines.

Paclitaxel (Taxol), a naturally occurring antimitotic agent, has shown significant cell-killing activity against human solid tumor cells through induction of apoptosis. The molecular mechanism underlying paclitaxel-induced apoptosis is not entirely clear. Using the unique inhibitory effect of glucocorticoids on paclitaxel-induced apoptosis, we recently discovered that paclitaxel-induced inhibitor kappaBalpha (IkappaBalpha) degradation and nuclear factor-kappaB (NF-kappaB) activation might contribute to the mediation of paclitaxel-induced apoptosis. In this study, using a novel IkappaBalpha phosphorylation inhibitor, we demonstrated that the blockage of paclitaxel-induced IkappaBalpha degradation inhibited apoptotic cell death in human breast cancer BCap37 and ovarian cancer OV2008 cell lines. Furthermore, in vitro kinase assays showed that the activity of IkappaB kinase (IKK), which is responsible for the phosphorylation and degradation of IkappaB proteins, was significantly activated by paclitaxel in these paclitaxel-sensitive tumor cells. Stable transfection of a mutant IkappaBalpha lacking Ser(32) and Ser(36) that was insensitive to IKK-mediated phosphorylation and degradation resulted in reduced sensitivity of tumor cells to paclitaxel-induced apoptosis. Moreover, we also found that the expression of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 1, an upstream regulator of IKK, was up-regulated by paclitaxel. These findings suggest that the activation of IKK might play a critical role in the regulation of paclitaxel-induced NF-kappaB activation that subsequently mediates paclitaxel-induced apoptotic cell death in solid tumor cells.

Antineoplastic Agents, Phytogenic↗

PubMed2002

Activation of nuclear factor-kappaB and not activator protein-1 in cellular response to nickel compounds.

The predominant exposure route for nickel compounds is by inhalation, and several studies have indicated the correlation between nickel exposure and respiratory cancers. The tumor-promoting effects of nickel compounds are thought to be associated with their transactivation of transcription factors. We have investigated the possible activation of activator protein-1 (AP-1) and nuclear factor KB (NF-kappaB) in mouse C141 epidermal cells and fibroblasts 3T3 and B82, and human bronchoepithelial BEAS-2B cells in response to nickel compound exposure. Our results show that NF-kappaB activity is induced by nickel exposure in 3T3 and BEAS-2B cells. Conversely, similar nickel treatment of these cells did not induce AP-1 activity, suggesting that nickel tumorigenesis occurs through NF-kappaB and not AP-1. We also investigated the role of NF-kappaB in the induction of Cap43 by nickel compounds using dominant negative mutant Ikappabeta kinase b-KM BEAS-2B transfectants.

Animals↗

PubMed2002

[Transmission disequilibrium test of DRD4 exon III 48bp variant number tandem repeat polymorphism and tic disorder].

OBJECTIVE: To investigate whether DRD4 exon III48 bp variant number tandem repeat(VNTR) polymorphism is associated with tic disorder. METHODS: One hundred and twenty-two nucleus families were collected using Structured clinical interview for genetic study of Tourette syndrome and related disorders for family-based association analysis of tic disorder and DRD4 exon III 48bp VNTR polymorphism. One hundred and twenty-two trios were divided into two groups: tic disorder group (82 trios of Tourette syndrome or chronic tic disorder, TS&CT) and tic disorder accompanied with attention deficit and hyperactivity disorder (ADHD) group (40 trios of Tourette syndrome or chronic tic disorder accompanied with ADHD, TS&ADHD). Transmission disequilibrium test (TDT), in addition to polymerase chain reaction and VNTR technique were conducted in 122 trios. RESULTS: There exist 5 alleles at this polymorphic locus in this sample including DRD4 exon III 48bp 2-6 repeats. No transmission disequilibrium was found between DRD4 exon III 48 bp VNTR and tic disorder (chi square=7.44, P 0.12); however, when the sample was divided into two groups, transmission disequilibrium was noticed between the cases of TS&ADHD and this locus by overall allele-wise analysis (chi square=11.74, P 0.02), and there exists transmission disequilibrium exclusively between 5 or 6 repeats of 48bp VNTR(longer alleles) by allele-wise analysis (chi square=10.57, P 0.032, chi square=6.13, P 0.01). No transmission disequilibrium was seen between TS&CT and DRD4 exon III 48bp VNTR(chi square=3.38, P 0.50). CONCLUSION: The results of this study have revealed an association between the longer alleles of DRD4 exon III 48bp VNTR polymorphism and tic disorder accompanied with ADHD, thus suggesting a possible genetic risk factor of tic disorder accompanied with ADHD in Chinese.

Adolescent↗

PubMed2002

[Uptake and distribution of Cu, Zn, Pb and Cd in maize related to metals speciation change in rhizosphere].

The behavior of heavy metals in terrestrial system and the mechanism of VAM plant in toleranting excessive heavy metals in soil were examined with VAM maize(Zea mays L.). After seven-week cultivation in sewage-sludging soil, the biomass of VAM (Glomus mosseae) maize was found 1.5 times higher than non-mycorrhizal one. Compared with non-mycorrhizal maize, the accumulation of Cu, Zn and Pb by mycorrhizal maize was reduced by 10%, 18% and 29%, respectively, but the accumulation of Cd was the same. The distribution and speciation change of Cu, Zn, Pb and Cd in rhizosphere of VAM and non-mycorrhizal maize were analyzed by using the technique of sequential extraction. Except a significant increase in exchangeable Cu in rhizosphere of VAM maize, the increased amount of test metals bound to organic matter, carbonates, iron and manganese oxides were significantly higher than those in rhizosphere of non-mycorrhizal maize, indicating that the speciation of metals in rhizosphere of mycorrhizal maize growing in contaminated soil tended to be relatively stable. Meanwhile, the influence of metal speciation in rhizosphere on its bioavailability as well as the mechanism of mycorrhizal plant in toleranting excess metals were also discussed.

Cadmium↗

PubMed2002

The possible correlation between activation of NF-kappaB/IkappaB pathway and the susceptibility of tumor cells to paclitaxel-induced apoptosis.

Paclitaxel (Taxol) is a naturally occurring antimitotic agent that has been shown to induce apoptosis in both leukemic and solid tumor cells, but many tumor cells exhibit a high resistance to paclitaxel. The mechanism of different susceptibility among tumor cells to paclitaxel-induced apoptotic cell death is not entirely clear. In this study, we identified and characterized two solid tumor cell lines, human breast tumor MCF7 cells and rat prostate tumor R3227 cells, which were resistant to paclitaxel-induced apoptosis. The results indicated that these tumor cells were highly resistant to paclitaxel-induced nucleosomal DNA fragmentation, but still sensitive to paclitaxel-induced microtubule bundling and cell cycle arrest at G2-M. This selective resistance of MCF7 and R3227 to paclitaxel suggests that mitotic arrest and apoptotic cell death might be two separate events, and paclitaxel-induced mitotic arrest may not always be followed by apoptotic cell death. Further, through comparative studies and analyses of a number of genes whose expression or activation may be involved in the regulation of apoptotic cell death or drug resistance, we found that paclitaxel induced the degradation of IkappaBalpha protein, which in turn activated NF-kappaB in paclitaxel-sensitive tumor cells, but such a paclitaxel-induced activation of the NF-kappaB/IkappaBalpha cascade was not observed in either MCF7 or R3227 cells. These findings suggest that the activation of NF-kappaB/IkappaBalpha signaling pathway might play an important role in determining the susceptibility of tumor cells to paclitaxel-induced apoptosis.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2002

[IRE_FINDER-computational search of iron response element in human and mouse UTRs].

The iron response element (IRE) is a highly conserved RNA stem loop structure. It is the binding site of iron regulatory protein (IRP). IRP binding to IRE is regulated by cellular iron. When cells are derived of iron, IRP binds IRE. If IRE is located at 5'UTR, IRP binding will inhibit translation initiation, else if IRE is at 3'UTR, IRP binding will stabilize mRNA and prevent it from degradation. So far all known IREs have C at the 1 position and G at the 5 position of the loop (C1G5 type). In vitro studies suggest that the U1A5 type IRE, which has U and A at the 1 and 5 loop position respectively, binds well to IRP. However, U1A5 type's in vivo existence is still elusive. IRE-IRP binding is involved in the regulation of iron metabolism, oxidative stress and possibly aging. Here we use an improved computation method performing a comprehensive search of IRE in human and mouse genes. We try to catalog potential human and mouse IRE containing genes, at the same time identify potential U1A5 IREs.

3' Untranslated Regions↗

PubMed2002

[Cryobiological characteristics of placental cord blood preserved in bioarchive auto-preserved liquid nitrogen system].

The aim of this study was to investigate the cryobiological characteristics of placental cord blood (PCB) cryopereserved by using BioArchive auto-preserved liquid nitrogen system (BioArchive system). After Hespan depletion of red blood cells, 5 ml mixture of DMSO and 10% Dextran 40 were added into 20 ml of enriched leukocyte. 53 PCB units were cryopreserved as following protocol: pre-freeze rate 10 degrees C/min, start freeze temperature -3 degrees C, end freeze temperature -10 degrees C to -15 degrees C, post freeze rate 2 degrees C/min, and end temperature -50 degrees C. After rapid thawing at 38 degrees C, the PCB were washed with 5% human serum albumin -10% Dextran 40 and centrifuged at 400 x g, 10 degrees C for 20 minutes. The results showed that the viability of nucleated cells post-thaw was (73.3 +/- 12.5)%, the CD34(+) cell content was (0.3 +/- 0.21)% for pre-freeze PCB and (0.45 +/- 0.36)% for post-t haw PCB. No significant difference for CFU-GM/-G/-GEMM counts was found between pre-freeze and post-thaw PCB. Thawed PCB contained in two compartments (20 ml and 5 ml) of a freezing bag showed similar viability and clonogenic capacity. Differential count of white blood cell was significantly changed. For post-thaw PCB, it was dramatically decreased for the percentage of granulocytes, and highly increased for the percentage of lymphocytes and monocytes. It was concluded that the condition for cryopreservation and thawing of PCB may be harmful to mature cells, and cells with large size, such as granulocyte, but suitable to lymphocyte and monocyte, especially for the cells with small size, such as CD34(+) cells.

Antigens, CD34↗