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Xiao-Ling Li

Publications and source records attributed to Xiao-Ling Li.

26 records · Page 2Linked to original sources

Expression of LRRC4 has the potential to decrease the growth rate and tumorigenesis of glioblastoma cell line U251.

BACKGROUND & OBJECTIVE: LRRC4 is a novel gene that the author has identified recently, which displayed significant downregulation in primary brain tumor biopsies. This study was designed to investigate if LRRC4 has the potential of suppressing brain tumor growth. METHODS: The full-length coding region of LRRC4 gene was subcloned into the expression vector pcDNA3.1, the recombinant was introduced into the glioblastoma cell line U251 by liposome transfection, and the U251 cells stably expressing LRRC4 gene were established by G418 selection. Furthermore, cell proliferation assay, soft agar assay, tumorigenesis assay were taken to examine the effect of LRRC4 expression on cell growth and tumor formation. RESULTS: U251 cells stably expressing full-length coding region of LRRC4 were established by lipofection-mediated transfection and selected for further study. Compared with the nontransfected and vector-transfected cells, the cells transfected with LRRC4 cDNA exhibited a significant increase of expression of LRRC4 mRNA by Northern blot analysis. Further, when cell proliferation was followed over several days, the cells expressing the transfected LRRC4 cDNA grew more slowly than nontransfected cells. Consistently, the cells transfected with LRRC4 exhibited markedly lower colony formation rate. These clones were injected into athymic nude mice who was killed after 40 days and the tumor sizes were evaluated. Tumor volume in mice was significantly smaller in the group of cells stably transfected with LRRC4 cDNA than in the control. CONCLUSION: LRRC4 gene may be transfected into the human glioblastoma cell line U251. The expression of LRRC4 in U251 cells may have the potential to suppress tumor cell growth and the tumorigenesis of U251 cell transplanted in nude mice.

Animals↗

[Biocompatibility of poly-l-lysine-modified silica nanoparticles].

BACKGROUND & OBJECTIVE: Poly-l-lysine-modified silica nanoparticle(PMS-NP) was a novel non-viral vector for gene delivery. The current study was designed to evaluate the biocompatibility of PMS-NP for its further utilization in vivo. METHODS: Cell transfection and flow cytometry were used to elucidate the delivery efficiency of plasmid DNA and antisense ODN mediated by PMS-NP in the presence of serum-containing medium. Subsequently, the biocompatibility of PMS-NP in vivo was evaluated using filtration assay of plasma proteins and erythrocyte aggregation assay. RESULTS: The abilities of PMS-NP to deliver plasmid DNA and antisense ODN in vitro clearly decreased in the presence of serum-containing medium. PMS-NP/DNA(ODN)complexes bound plasma proteins and triggered erythrocyte aggregation. CONCLUSION: PMS-NP might interact with plasma proteins, resulting in decreased transfection efficiency in vitro. And filtration assay of plasma proteins and the erythrocyte aggregation assay demonstrated that the interaction of PMS-NP with plasma proteins and erythrocytes might play a negative role in gene transfection efficiency in vivo. And its biocompatibility needs to be further improved.

Animals↗

[Information behavior of 7 STR loci on chromosome 9p in gene scanning].

To get genotype and allele frequency distributions of seven short tandem repeat (STR) loci of chromosome 9p,D9S288,D9S157,D9S1748,D9S171,D9S161,D9S1817 and D9S1805 in Chinese Han population in Hunan area,blood samples were collected from the random Han individual in Hunan and the whole genomic DNA was extracted.STR loci were amplified by multiplex-PCR technique and genotyped by ABI 377 sequencer.Seventy-five alleles were detected,with frequencies ranging from 0.002 to 0.800,and constituted 243 genotypes. All the seven loci met Hardy-Weinberg equilibrium. The statistical analysis of seven STR loci showed H(heterozygosity) ranging from 0.347 to 0.844,DP(discrimination power) ranging from 0.346 to 0.841,PPE(probabilities of paternity exclusion) ranging from 0.308 to 0.738 and PIC(polymorphic information content) ranging from 0.328 to 0.822. The result indicated that there was a significant difference between Han ethnic group and the white and the black.

English Abstract↗

Profiling genes differentially expressed in NGX6 overexpressed nasopharyngeal carcinoma cells by cDNA array.

PURPOSE: To investigate the role of the NGX6 gene in carcinoma proliferation and profile the downstream genes regulated by NGX6 in a nasopharyngeal carcinoma (NPC) cell line. METHODS: We established a NPC cell line with NGX6 overexpression by gene transfection. Subsequently, a high-density cDNA array was used to identify differentially expressed genes in NGX6-overxepressed cells. Four differentially expressed genes or EST(expressed sequence tags) were examined using Northern blot. Furthermore, flow cytometry was employed to analyze the percentages of cells in the G(0)-G(1), S, and G(2)-M phase of the cell cycle in a NGX6 overexpression cell line. RESULTS: Fifty-five genes and ESTs were differentially expressed after NGX6 transfection in a cDNA array assay. Several genes related to cell cycle and transcription regulation were identified using this technique. Flow cytometry analysis showed NGX6 overexpression can increase the length of the G(1) phase of the cell cycle in NPC cells. CONCLUSION: We demonstrated the existence of a panel of genes that can be regulated by NGX6. Overexpression of NGX6 can influence the distribution of the cell cycle in NPC cells. Further studies are necessary to elucidate the exact function of these genes and their relationship to NGX6 expression.

Carcinoma↗

Proteasomes modulate conjugation to the ubiquitin-like protein, ISG15.

ISG15 is a ubiquitin-like protein that is induced by interferon and microbial challenge. Ubiquitin-like proteins are covalently conjugated to cellular proteins and may intersect the ubiquitin-proteasome system via common substrates or reciprocal regulation. To investigate the relationship between ISG15 conjugation and proteasome function, we treated interferon-induced cells with proteasome inhibitors. Surprisingly, inhibition of proteasomal, but not lysosomal, proteases dramatically enhanced the level of ISG15 conjugates. The stimulation of ISG15 conjugates occurred rapidly in the absence of protein synthesis and was most dramatic in the cytoskeletal protein fraction. Inhibition of ISG15 conjugation by ATP depletion abrogated the proteasome inhibitor-dependent increase in ISG15 conjugates, suggesting that the effect was mediated by de novo conjugation, rather than protection from proteasomal degradation or inhibition of ISG15 deconjugating activity. The increase in ISG15 conjugates did not occur through a stabilization of the ISG15 E1 enzyme, UBE1L. Furthermore, simultaneous modification of proteins by both ISG15 and ubiquitin did not account for the proteasome inhibitor-dependent increase in ISG15 conjugates. These findings provide the first evidence for a link between ISG15 conjugation and proteasome function and support a model in which proteins destined for ISG15 conjugation are proteasome-regulated.

Cell Line↗

Restoration of T cell-specific V(D)J recombination in DNA-PKcs(-/-) mice by ionizing radiation: The effects on survival, development, and tumorigenesis.

DNA-dependent protein kinase (DNA-PK) is a DNA-activated nuclear serine/threonine protein kinase. DNA-PK consists of a heterodimeric Ku subunit (composed of a 70 and 86 kD subunit) which binds DNA ends and targets the catalytic subunit DNA-PKcs to DNA strand breaks. DNA-PK plays a major role in the repair of double-strand breaks (DSB) induced in DNA after exposure to ionizing radiation. To better understand the nature of DNA repair defect associated with DNA-PKcs deficiency, we have established DNA-PKcs(-/-) mouse embryo fibroblast cell lines and DNA-PKcs(-/-) null mice, and investigated the response of these mutant cells and mice to DNA damage. DNA-PKcs(-/-) cells are hypersensitive to gamma-irradiation, as evidenced by their low survival as assayed by colony formation efficiencies. Consistent with the radiation hypersensitive phenotype of the cell lines, DNA-PKcs(-/-) mice also display an extreme radiosensitivity, characterized by enhanced mortality after gamma-irradiation. Treatment of newborn DNA-PKcs(-/-) mice with sublethal doses of ionizing radiation restores T cell receptor (TCR) beta recombination and T cell maturation. However, radiation does not restore B cell development. All these mice eventually developed thymic lymphoma. These observations suggest an interrelationship between DSB repair, V(D)J recombination and lymphomagenesis, and provide an in vivo model to elucidate the critical pathways between the regulation of DNA DSB repair, V(D)J recombination, and the molecular mechanism of lymphoid neoplasia.

Animals↗

Single-nucleotide polymorphisms in NGX6 gene and their correlation with nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is rare in most parts of the world, but prevalent in southern China. Recently, a NGX6 gene was cloned, which is located in the region of minimal heterozygosity deletion at 9p21.3-22.1 and is down-expressed in NPC. The latest results suggest that the NGX6 gene is a candidate tumor suppressor for NPC. A correlation study using 2 single-nucleotide polymorphisms (SNPs) within NGX6 gene by means of dynamic allele specific hybridization (DASH) was performed in 105 unrelated case subjects and 183 control subjects which matched to the NPC cases in age, sex and residence. Significant results were obtained for one SNP mark (rs879284), which was located at -237 bp 5' up-stream of NGX6 gene, and the relative risk of this SNP mark was 3.93 (genotype CT) and 2.27 (genotype TT). The result has proved again that NGX6 gene may play a certain role in oncogenesis and development of nasopharyngeal carcinoma. The SNP mark rs879284 may influence on the expression of NGX6 gene due to its location on chromosome.

Adult↗

In vitro permeation of tetramethylpyrazine across porcine buccal mucosa.

AIM: To examine the in-vitro transport route of tetramethylpyrazine (TMP) across porcine buccal mucosa and to investigate the effects of drug concentration, pH in donor chamber, and 1-octanol/buffer partition coefficient on transbuccal permeation. METHODS: In-vitro permeation of TMP through porcine buccal mucosa was studied by using in-line flow through diffusion cells at 37 . The permeability of TMP was evaluated at different donor pH and drug concentration. Permeability of unionized (Pu) and ionized TMP (Pi) was calculated by using the Scientist software. RESULTS: The steady state flux of TMP increased linearly with the donor concentration (r2=0.96) at pH 7.4. The permeability and the partition coefficient increased with pH. Pu and Pi were 9.05 x 10(-6) cm.s(-1) and 2.99 x 10(-7) cm.s(-1), respectively. The total permeability coefficient increased with the fraction of unionized form. CONCLUSION: TMP permeated through buccal mucosa by a passive diffusion process. The partition coefficient and pH dependency of drug permeability indicated that the drug was transported mainly via the transcellular route by a partition mechanism.

Absorption↗