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Wang Li-jun

Bio: Wang Li-jun is an academic researcher from Qingdao University. The author has contributed to research in topics: Incubator & Cytokeratin. The author has an hindex of 2, co-authored 2 publications receiving 10 citations.

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Journal Article
TL;DR: The novel endometrial adenocarcinoma cell line is successfully established and the expression of cytokeratin was positive in the cells.
Abstract: Objective To establish human endometrial adenocarcinoma cell line.Methods Tumor tissues from 1 case with well differentiated endometrial adenocarcinoma were made into single-cell suspension and cultured in DMED/F-12 medium supplemented with 10% fetal bovine serum.The morphology of the cells was observed by inverted microscope.The immunofluorescent staining technique was used to detect cytokeratin in endometrial carcinoma cells.Results The cells were subcultured more than 50 generations,monolayer cultured cells were polygonal in shape and had a tendency to pile up without contact inhibition.The expression of cytokeratin was positive in the cells.Conclusion The novel endometrial adenocarcinoma cell line is successfully established.

8 citations

Journal Article
Wang Li-jun1
TL;DR: The evaluation indexes system of the incubating capacity of the business incubator is established and got the evaluation method system by factor analysis.
Abstract: On the basis of definition of the connotation and the incubating capacity of the business incubator, the evaluation indexes system of the incubating capacity of the business incubator is established and got the evaluation method system by factor analysis. Using these indexes system, the incubating ability is evaluated of National Business Incubators of ten different centuries in 2005.

2 citations


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Journal ArticleDOI
TL;DR: Results indicate that the cyclic expression of laminin and COL-4 in basement membrane-like structures of endometrial epithelium may regulate the endometrian epithelial remodeling and embryo implantation during the menstrual cycle.
Abstract: We investigated the expression and function of laminin and type IV collagen (COL-4) in the human endometrial epithelium throughout the menstrual cycle. Their expression was demonstrated by immunohistochemistry, while cytological analysis of the human endometrial epithelial cell line HHUA cultured on laminin- or COL-4-coated plates provided information on their roles in cell proliferation, structure and apoptosis. Laminin and COL-4 were detected in subepithelial basement membrane-like structures and their expression levels varied throughout the menstrual cycle. Laminin expression was significantly decreased in secretory phase endometrial surface epithelium, while COL-4 expression was significantly decreased in late proliferative phase endometrial epithelium and in vascular endothelium. The morphology of proliferating HHUA cells varied depending on the extracellular matrix component coated on the culture plates. COL-4 strongly inhibited cell proliferation of HHUA cells and enhanced Fas antigen (CD95)-mediated apoptosis, while laminin inhibited Fas-mediated apoptosis. These results indicate that the cyclic expression of laminin and COL-4 in basement membrane-like structures of endometrial epithelium may regulate the endometrial epithelial remodeling and embryo implantation during the menstrual cycle.

30 citations

Journal ArticleDOI
TL;DR: Leptin at a physiological serum concentration, may regulate the remodeling of the human endometrial epithelium by stimulating cell proliferation and enhancing the Fas-specific intracellular apoptotic signaling pathway.
Abstract: The biological functions of leptin in the human endometrial epithelium were investigated using the human endometrial epithelial cell line, HHUA. Specifically, the effects of leptin on the proliferation and apoptosis of HHUA cells induced by treatment with anti-Fas IgM or anticancer drugs were examined. RT-PCR detected the expression of four leptin receptor isoform mRNAs in the cells and flow cytometric analysis revealed cell surface expression of the leptin receptor molecules. Leptin stimulated HHUA cell proliferation in a dose-dependent manner at concentrations below the normal serum leptin level. Leptin enhanced anti-Fas IgM-mediated growth inhibition and DNA fragmentation, but did not enhance the expression of either Fas antigen or Fas ligand. Moreover, leptin had no effect on anticancer drug-induced apoptosis. Based on these results, leptin at a physiological serum concentration, may regulate the remodeling of the human endometrial epithelium by stimulating cell proliferation and enhancing the Fas-specific intracellular apoptotic signaling pathway.

29 citations

Journal ArticleDOI
TL;DR: The results indicate that the cell death signals induced by mitomycin, pirarubicin and bleomycin are distinctly different from the Fas-mediated apoptotic signals, that acquisition of 5FU-resistance can occur without any large chromosomal deletions or rearrangements, and that there are several possible molecular changes during the acquisition of 4-fluorouracil (5FU)-resistance.
Abstract: To investigate acquired 5-fluorouracil (5FU)-resistance in cancer cells, we established four monoclonal 5FU-resistant cell lines from human endometrial adenocarcinoma cells by long-term 5FU-exposure cultures and limiting dilution cultures. The established subclones exhibited 5-25 times greater 5FU-resistance than the parent cells, and showed suppression of 5FU-induced DNA fragmentation. All four 5FU-resistant subclones were 25-125 times more resistant to SN38, 4-hydroxy-cyclophosphamide, paclitaxel and etoposide than the parent cells while none of the four subclones showed resistance to mitomycin. Two of the four subclones showed no resistance to pirarubicin and bleomycin. Although all four 5FU-resistant subclones were 5-25 times more resistant to anti-Fas IgM than the parent cells, the resistance levels to anti-Fas IgM of the individual subclones did not coincide with the strengths of their multidrug resistance. Karyotyping analyses revealed that the parent cells and the three 5FU-resistant subclones examined had normal 46XX karyotypes. These results indicate that the cell death signals induced by mitomycin, pirarubicin and bleomycin are distinctly different from the Fas-mediated apoptotic signals, that acquisition of 5FU-resistance can occur without any large chromosomal deletions or rearrangements, and that there are several possible molecular changes during the acquisition of 5FU-resistance. The established cell lines represent useful tools for investigating the mechanisms and treatments of acquired 5FU-resistance.

8 citations

Journal ArticleDOI
TL;DR: 5FU-combined chemotherapy with DAPK siRNA transfection may show stronger anticancer effects on patients with endometrial adenocarcinoma than does chemotherapy alone, and results indicate that etoposide-stimulated cell death signals may share or include TRAIL-mediated apoptotic signals.
Abstract: Targeted knockdown of the death-associated protein kinase (DAPK) expression in the endometrial adenocarcinoma HHUA cells reportedly induces cell death by enhancing the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in an autocrine/paracrine manner. This suggests that endogenous DAPK is a potential candidate for a molecularly targeted anticancer therapy for patients with endometrial adenocarcinoma. To investigate the role of endogenous DAPK in anticancer drug sensitivity, we examined effects on cellular anticancer drug sensitivities of transfections with 5 different specific DAPK small-interfering RNAs (siRNAs) into HHUA cells. DAPK siRNA transfections strongly enhanced 5-fluorouracil (5FU)-sensitivity, but not etoposide-sensitivity, of HHUA cells compared with control siRNA-transfected cells. These results indicate that etoposide-stimulated cell death signals may share or include TRAIL-mediated apoptotic signals, and that 5FU-stimulated cell death signals may be independent from TRAIL-mediated apoptotic signals induced by DAPK siRNA transfections. Moreover, 5FU-combined chemotherapy with DAPK siRNA transfection may show stronger anticancer effects on patients with endometrial adenocarcinoma than does chemotherapy alone.

7 citations

Journal ArticleDOI
TL;DR: Results indicate that danazol may regulate endometrial epithelial cell proliferation and apoptosis within normal physiology.
Abstract: Local danazol therapy reduces the signs and symptoms of endometriosis without inhibition of regular ovulation and menstruation and without atrophic changes to the endometrium or vaginal wall. It has been suggested that danazol has possible non-cytotoxic direct actions on eutopic endometrial cells and endometriotic cells. We have investigated the direct effects of danazol on a human endometrial epithelial cell line, HHUA, which is believed to retain many normal intracellular signaling pathways. A thoroughly dissolved solution of danazol enhanced Fas-mediated apoptosis in HHUA cells without inhibiting cell proliferation. Semi-quantitative flow cytometric analysis revealed that danazol did not enhance cell surface expression of Fas antigens. The enhancement of Fas-mediated apoptosis by endometrial cytokines such as EGF, IL-1beta and interferon-gamma was not additively enhanced by danazol; nor did danazol enhance growth suppression by anticancer drugs such as paclitaxel, carboplatin and 5-fluorouracil. Moreover, danazol did not enhance the irradiation-induced cell growth suppression of radiation-sensitive human cervical squamous cancer ME180 cells. These results indicate that danazol may regulate endometrial epithelial cell proliferation and apoptosis within normal physiology.

6 citations