Publications by authors named "Jin-Zhao Li"

p53 plays an important role in drug responses by regulating cell cycle progression and inducing programmed cell death. The C-terminal of p53 self-regulates the protein negatively; however, whether it affects the sensitivity of cancer cells to anticancer drugs is unclear. In this study, two experimental methods were used to compare the sensitivity to anticancer drugs of human lung 801D cancer cells transfected with adenovirus bearing either full-length p53 or the deleted-C-terminal p53 in vivo.

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Purpose: To investigate the changes and the significance of caveolin-1 gene and protein in tongue squamous cell carcinoma(TSCC).

Methods: Immunohistochemical staining and in situ hybridization were used to detect the changes of caveolin-1 gene and the protein in 92 TSCCs and their adjacent normal tissues. The data were analyzed with SPSS10.

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Objective: To investigate the changes and significance of cell apoptosis and Fas/FasL gene in pulmonary fibrosis.

Methods: Forty mice were divided into two groups randomly, each group contained twenty mice. TUNEL, immunohistochemistry and in situ hybridization were used to detect the change of cell apoptosis, Fas/FasL mRNA and protein in mice with pulmonary fibrosis caused by bleomycin.

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Objective: To detect the levels of prostaglandin E2 (PGE2) and interleukin-12 (IL-12), IL-13 in the bronchoalveolar lavage fluid (BALF) and the serum of patients with idiopathic pulmonary fibrosis (IPF) and to investigate the significance of their change in the pathogenesis of IPF.

Methods: Radioimmunoassay (RIA) and enzyme-linked immunoadsorbent assay (ELISA) were used to detect the levels of PGE2 and IL-12, IL-13 in the BALF and the serum of patients with IPF.

Results: In the BALF of patients with IPF, the levels of PGE2 (591 +/- 88) ng/L and IL-13 (38 +/- 5) ng/L were higher than that of the control group (P < 0.

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Objective: To study the effect of extraneous p53 gene with deletion of c-terminal 356 - 393 amino acids on inhibition of malignant phenotype of human lung cancer cell line.

Methods: Recombinant plasmid pEGFP-p53 (del) with codon deletion of c-terminal 37 amino acids from 393 to 356 region and pEGFP-p53 (wild type) were constructed. The human lung cancer cell line 801D served as a receipt cell had p53 deletion and mutation at 248 codon.

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