AIM,To verify whether p73;a homologue of p53,which supposed]y acts as a tumor suppressor gene in neuroblastoma,might also be a tumor suppressor in non-small cell lung cancer.METHODS:The allelic expres-sion of p73 in the six non-small cell lung cancer cell lines was studied by Sty I polymorphism analysis.The P73 gene ex.pressions in these six cell lines were examined by reverse transcription-PCR,the expressions of P73 protein in the five cell lines inducing tumor8 were also determined by immunohistochemistry.RESULTS:Homozygous allelic expression was dem.onstrated in all six cell lines and the GC/GC genotype Was the predominant type.Complete loss of the p73 expression both at mRNA and the protein level was revealed.CONCLUSION:Taken together,our data suggest that p73 might play a role as a tumor suppressor gene in human non-small cell lung cancer cell lines.

AIM: To explore the effect of collagen and C-erbB-2 protein on the adhesion and the proliferation in hepatocellular carcinoma cells.METHODS: Hepatocellular carcinoma cell line(HepG-2) identified to positive for C-erbB-2 gene was used to study the adhesion and the growth feature by the action of rat tail collagen and C-erbB-2 antibody.RESULTS: The action of rat tail collagen to potentiated the adhesion in HepG-2 cells was significantly but no proliferation effect was observed. C-erbB-2 antibody inhibited the adhesion and proliferation of HepG-2 cells and also abolished the potentiated effect of rat tail collagen on the adhesion in HepG-2 cells.CONCLUSIONS: The signaling transduction mediated by C-erbB-2 protein was correlated to the adhesion and the proliferation of HepG-2. The blockage of C-erbB-2 gene signal transduction may be a strategic target to the treatment of liver cancer in the future.

AIM: To examine the effect of insulin on the proliferation of human hepatocellular carcinoma cell and its possible mechanisms. METHODS: The human hepatocellular carcinoma cell line(HepG-2) was used to study the changes in calcium ion across plasma membrane (Ca 2+ APM)under the action of insulin by the assay of atomic absorption spectrum, and in the proliferation under the action of insulin and calcium ion antagonist (isoptin). RESULTS: The influx of Ca 2+ APM and the proliferation was increased after insulin administration, but the proliferation was inhibited by isoptin. CONCLUSION: Changes in the homeostasis of calcium ion across plasma membrane was involved in the effect of insulin on the proliferation of human hepatocellular carcinoma.

AIM:To study whether three kinds of rabbit corneal cells can grow well on fibrin glue (FG) constructed in vitro, and investigate the feasibility of FG for the scaffold of cell sheet engineering. METHODS: Three kinds of corneal cells were seeded on FG which was produced in vivo. Cell growth on FG was examined as follows: (1) by inverted microscope; (2) histologically by hematoxylin and eosin; (3) by scanning electron microscopy. RESULTS: Fibrin glue prepared was smooth and transparent. With cell growth, FG degradated partly, then obtained cell sheet engineering only with a small amount of FG. Corneal cells generated well on the fibrin glue in vitro and maintained the physiological state of cells. Corneal epithelial cells formed unilaminar and stratified layers and cellular joins. Corneal endothelial cells formed round or polygon, the same size cells and lined up tightly. Corneal stroma cells formed triangle and arborization, cell-cell junction was obvious, and formed network link. CONCLUSION: Fibrin glue is well compatible with three kinds of corneal cells, which can construct tissue engineered cell sheet with fibrin glue, so as to reconstruct ocular surface.

AIM: To investigate whether protein kinase C (PKC) is involved in the proliferation and the telomerase expression in human hepatocellular carcinoma cells. METHODS: Human hepatocellular carcinoma cells (BEL-7402) were treated with exogenous phorbol-12-myristate-13-acetate (PMA, PKC activator) and staurosporine (SP, PKC inhibitor) for 48 hours. The techniques of cell culture and the telomeric repeat amplification protocol silver staining in combination with computer image scanning system in vitro were used to observe the variations of the growth and the telomerase expression. RESULTS: The proliferative potential of BEL-7402 cells was decreased by the action of PMA as well as SP, and the telomerase expression was also inhibited by PMA and SP. CONCLUSION: Our findings suggest that the proliferation of human hepatocellular carcinoma cells and the telomerase expression may be related to PKC. [

AIM: To investigate the effects of Xiaochaihutang (XCH), a Chinese medicine, and danazol on angiogenesis factor and microvessel density (MVD) of endometriosis (EM). METHODS: EM rats were treated with XCH, Danazol (D), and XCH plus D (group S) for 4 weeks, respectively. The histomorphology and volumes of ectopic endometrium were observed, the amount of macrophages in peritoneal fluid of EM model rats was counted, the concentration of interleukin-8 (IL-8) and tumor necrosis factor-? (TNF-?) of EM model rats in serum, peritoneal fluid, and supernate of cultured macrophages were measured. In addition, vascular endothelial growth factor (VEGF) was detected in ectopic endometrium by immunohistochemical SABC technique, MVD was determined by immunostaining for CD34. Similar studies were performed in rats without treatment (U group) and another group with sham operation (C). RESULTS: Compared with U group, XCH group, D group, and S group displayed a significant atrophy of ectopic endometrium, reduced number of endometrial glands, decreased macrophage amounts and low concentrations of IL-8 and TNF-? in blood, peritoneal fluid, and supernate of cultured macrophages . The expression of VEGF and MVD of ectopic endometrium in U group were significantly higher than that of C group. After treatment, they all decreased significantly, especially in S group. CONCLUSIONS: Both XCH and danazol can affect angiogenesis of EM model rats, cause an obvious atrophy in ectopic endometrium. XCH in combination with danazol can enhance the inhibitory effect on angiogenesis of EM model rats.

AIM: To detect the expression of cytoplasmic inhibitor of apoptosis protein 2 (c-IAP2) and growth arrest-specific gene 1 (GAS1) in Hodgkin's lymphoma (HL) and anaplastic large cell lymphoma (ALCL) and to investigate the role of two genes in the pathogenesis of HL and ALCL.METHODS: HE staining,the antibodies CD30,CD15,CD45RO and CD20 were used to screen the cases of HL and ALCL from 288 cases of lymphoma. The clarified HL and ALCL were subjected for immunohistochemical staining by SP and ABC methods to analyze the expression of c-IAP2 and GAS1. RESULTS: ①The positive rate of c-IAP2 in HL was 25/26(96.1%) while that in ALCL was 6/19(31.6%),there presented statistic significance between HL and ALCL groups( P

AIM: To obverse the expression and localization of urocortin on ultrathin cryosections of syncytiotrophoblast of human term placenta with immunocytochemistry technique under transmission electron microscope. METHODS: The human term placenta tissue from Cesarean delivery and normal labor were fixed in 4% paraformaldehyde, and then divided into two parts. One part was for regular immunocytochemistry under microscope, and the other part was used to prepare ultrathin cryosections for immunocytochemistry under transmission electron microscope. RESULTS: 1.Uroncortin mainly distributed in cytoplasm of syncytiotrophoblast of human term placenta under microscope. Urocortin also appeared in cytoplasm in some stromal cells. 2. Under transmission electron microscope, the anti-urocortin gold particles were observed in cytoplasm of syncytioptrophoblast ultrathin cryosections and sited on rough-surfaced endoplasmic reticulum. The anti-urocortin gold particles also appeared on nucleus and nuclear membrane of syncytiotrophoblast. CONCLUSION: Syncytiotrophoblast of human term placenta synthesized and secreted urocortin. The internalization of urocortin within syncytiotrophoblast nuclear indicates that urocortin may act as intracrine.

AIM: This study is based on the result of the study in HL and ALCL employing gene chip technique, in which writer found that there was distinctly different expression of caspase-4 between HL and ALCL cell lines at the level of mRNA. From the point of view, we try to identify at the level of protein whether there is different expression of this gene in HL and ALCL tissues as well. METHODS: HE staining, the monoclonal antibodies CD30 (BerH2), CD15 (C3D-1), CD20 (L26) and CD45RO (UCHL1) were used for selecting the cases of HL and ALCL. Specific high affinitive anti-caspase-4 polyclonal antibody was used by immunohistochemical staining to analyze the expression of caspase-4 in 18 cases of HL and 15 cases of ALCL. RESULTS: The expression of caspase-4 demonstrated a strong positive staining in all ALCL cases (15/15,100%), whereas negative in 16 HL cases (88 8%), while other two cases were weakly stained (11 2%), showing a distinct difference (P

Epithelial membrane protein 3 (EMP3) is a trans-membrane signaling molecule with important roles in the regulation of apoptosis, differentiation and invasion of cancer cells, but the detailed is largely still unknown. We analyzed the mRNA levels and methylation statuses of EMP3 in 63 primary breast carcinomas and assessed their correlations with clinicopathologic variables. The expression of EMP3 mRNA in primary breast carcinomas was significantly higher than the expression of 20 normal breast tissues (p<10(-7)). EMP3 overexpression in breast carcinomas was significantly related to histological grade III (p=3.9X10(-7)), lymph node metastasis (p= 0.003), and strong Her-2 expression (p=3.3X10(-6)). Hypermethylation frequencies of EMP3 were detected in 36.5% of breast carcinomas by methylation-specific polymerase chain reaction. However, no significant correlations were found between methylation status of EMP3 and mRNA expression levels as well as other clinical parameters. In conclusion, EMP3 may be a novel marker of tumor aggressiveness. Overexpression of EMP3 in primary breast carcinoma is not associated with DNA methylation.
Adult ; Breast Neoplasms/*genetics/pathology ; Carcinoma/*genetics/pathology ; DNA Methylation ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphatic Metastasis ; Membrane Glycoproteins/*genetics/metabolism ; Middle Aged ; Neoplasm Staging ; RNA, Messenger/metabolism ; Receptor, erbB-2/genetics/metabolism ; Severity of Illness Index