The Experts below are selected from a list of 379908 Experts worldwide ranked by ideXlab platform

Ni Jian-q - One of the best experts on this subject based on the ideXlab platform.

  • The expression and significance of p120 catenin in pancreatic Carcinoma Cell lines
    Chinese clinical oncology, 2009
    Co-Authors: Ni Jian-q
    Abstract:

    Objective:To investigate the expression of p120(p120ctn) catenin and VEGF in pancreatic Carcinoma Cell lines, and the relationship between the expression of p120ctn and the biological behaviour of the Cell lines. Methods:The expression of p120ctn and VEGF in five pancreatic Carcinoma Cell lines and normal pancreatic Cell(PSCs) were detected by RT-PCR and Western blotting analysis; selected panc-1 and Patu8988 which have visible differential expression of p120ctn and VEGF to detect the biological behaviour using transwell test. Results:In comparison with PSCs, p120ctn were overexpressed in pancreatic Carcinoma Cell lines; moreover, it had different expression in different Cell lines. In the same Cell lines,the expression level of p120ctn were correlated with VEGF. There had inverse correlation of p120ctn's expression with the invasion and migration of pancreatic Carcinoma. Conclusion:Expression of p120ctn is increased in the pancreatic Carcinoma Cell lines and correlated with expression of VEGF. Overexpression of p120ctn may play a role in invasion and migration capability of pancreatic Carcinoma.

Tomohiko Koyanagi - One of the best experts on this subject based on the ideXlab platform.

  • the significance of ras guanine nucleotide exchange factor son of sevenless protein in renal Cell Carcinoma Cell lines
    The Journal of Urology, 1997
    Co-Authors: Nobuo Shinohara, Tohru Harabayashi, Motoyoshi Tanaka, Ataru Sazawa, Yoshifumi Ogiso, Tomohiko Koyanagi
    Abstract:

    AbstractPurpose: The aim of the present study is to clarify the significance of the Ras guanine-nucleotide exchange reaction in the proliferation of human renal Cell Carcinoma Cell lines.Materials and Methods: We examined the expression of human son of sevenless-1 (hSos-1) protein and the epidermal growth factor (EGF) receptor in human Cell Carcinoma Cell lines by Western blot analysis. Additionally, a dominant negative H-ras mutant, N116Y, which is known to inhibit the Ras guanine-nucleotide exchange reaction, was transfected into these Cell lines by lipofection.Results: Human renal Cell Carcinoma Cell lines expressed much higher amounts of the EGF receptor and hSos-1 protein than normal kidney tissue. Moreover, the N116Y ras mutant could strongly suppress Cellular proliferation in these Cell lines.Conclusions: Augmentation of the Ras guanine-nucleotide exchange reaction might be essential to the proliferation of human renal Cell Carcinoma Cells.

Masaki Saito - One of the best experts on this subject based on the ideXlab platform.

  • Tenascin induction in tenascin nonproducing Carcinoma Cell lines in vivo and by TGF-β1 in vitro
    Journal of Cellular Physiology, 1994
    Co-Authors: Takao Sakai, Hisaaki Kawakatsu, Masatsugu Ohta, Masaki Saito
    Abstract:

    Tenascin, a novel six-armed extraCellular-matrix glycoprotein, is expressed in a temporally and spatially restricted pattern during carcinogenesis in association with stromal-epithelial interactions. In this study, we have tested the hypothesis that tenascin expression depends upon the change of the Cellular environment from in vitro to in vivo. The distribution and alterations in the expression of tenascin were compared between in vitro and in vivo studies in a variety of human epithelial- and nonepithelial-derived Cell lines. When Cell lines were transplanted into nude mice, all xenografts induced host-mouse-stroma-derived tenascin. Four Carcinoma-derived Cell lines and all sarcoma-derived lines, which secreted tenascin in vitro, were found to produce human tenascin after transplantation. Furthermore, three Carcinoma-derived Cell lines, A431, HEp-2, and MCF7, which did not synthesize tenascin in vitro, did synthesize human tenascin after transplantation. These tenascin nonproducing Carcinoma Cell lines did not express tenascin mRNA in vitro. The addition of TGF-β1 to the culture medium induced the synthesis and secretion of tenascin, but TGF-β2 and bFGF were less effective. TGF-β1 also induced other extraCellular-matrix components, fibronectin and laminin. TGF-β1 did not induce tenascin in tenascin nonproducing Carcinoma Cell lines, such as WiDr and A549, in which human tenascin was not induced after transplantation. We have established an in vitro system in which tenascin is induced by the diffusible factor TGF-β1. This system could shed light on the mechanism of induction of human tenascin observed in vivo in tenascin nonproducing Carcinoma Cell lines. © 1994 wiley-Liss, Inc.

Soon Chul Myung - One of the best experts on this subject based on the ideXlab platform.

  • Different effect of protein kinase B/Akt and extraCellular signal-regulated kinase inhibition on trichostatin A-induced apoptosis in epithelial ovarian Carcinoma Cell lines
    Molecular and Cellular Biochemistry, 2011
    Co-Authors: Eun-ra Jang, Soon Chul Myung
    Abstract:

    Histone deacetylase inhibitor-induced apoptosis in cancer Cells may be mediated by the Ras/Raf/MEK/ERK and protein kinase B/Akt signaling pathways. However, inhibition of ERK and Akt activity has different effects on proliferation and apoptosis in cancer Cells. We assessed and compared the inhibitory effects of Akt and ERK pathways on the apoptotic effect of trichostatin A using the human epithelial Carcinoma Cell lines OVCAR-3 and SK-OV-3. Trichostatin A induced nuclear damage, decrease in Bid and Bcl-2 protein levels, increase in Bax levels, cytochrome c release, activation of caspases (8, 9, and 3) and increase in tumor suppressor p53 levels. Akt inhibitor potentiated trichostatin A-induced apoptosis-related protein activation and Cell death, whereas ERK inhibitor exhibited an additive toxic effect. These results suggest that the Akt and ERK inhibitors may have a differential effect on trichostatin A-induced apoptosis in human epithelial ovarian Carcinoma Cell lines. Akt inhibitor may potentiate the apoptotic effect of trichostatin A on ovarian Carcinoma Cell lines by increasing the activation of the caspase-8-dependent pathway and the mitochondria-mediated Cell death pathway, leading to caspase activation. In contrast, ERK inhibitor may exhibit an additive toxic effect on trichostatin A toxicity by increasing apoptosis-related protein activation.

  • 18β-Glycyrrhetinic acid potentiates apoptotic effect of trichostatin A on human epithelial ovarian Carcinoma Cell lines.
    European journal of pharmacology, 2010
    Co-Authors: Jae Chon Yang, Eun-ra Jang, Soon Chul Myung
    Abstract:

    The licorice-derived compounds glycyrrhizin and 18β-glycyrrhetinic acid have been shown to induce apoptosis in various cancer Cells. However, the effect of these licorice compounds on the apoptotic effect of histone deacetylase inhibitors in epithelial ovarian Carcinoma Cells has not been determined. We assessed the effect of 18β-glycyrrhetinic acid on trichostatin A-induced apoptosis in the human epithelial Carcinoma Cell lines OVCAR-3 and SK-OV-3. Trichostatin A induced nuclear damage, decreased Bid and Bcl-2 protein levels, increased in Bax levels, induced cytochrome c release, activated caspase-8, -9 and -3, and increased tumor suppressor p53 levels. 18β-Glycyrrhetinic acid potentiated the trichostatin A-induced apoptosis-related protein activation and Cell death. Unlike 18β-glycyrrhetinic acid, up to 25 μM of the pro-compound glycyrrhizin did not induce Cell death and did not affect trichostatin A-induced apoptosis. The results suggest that 18β-glycyrrhetinic acid may potentiate the apoptotic effects of trichostatin A against ovarian Carcinoma Cell lines by increasing the activation of the caspase-8-dependent pathway as well as the activation of the mitochondria-mediated Cell death pathway, leading to activation of caspases. 18β-Glycyrrhetinic acid may enhance the therapeutic effect of trichostatin A against epithelial ovarian adenoCarcinoma.

Stefan Rosewicz - One of the best experts on this subject based on the ideXlab platform.

  • Stromelysin 3 is overexpressed in human pancreatic Carcinoma and regulated by retinoic acid in pancreatic Carcinoma Cell lines
    Gut, 1998
    Co-Authors: Zofia Von Marschall, Ernst-otto Riecken, Stefan Rosewicz
    Abstract:

    Background—Matrix metalloproteinases play an important role in the control of local tumour growth and metastasis of human pancreatic cancer. Aims—To examine expression of recently discovered stromelysin 3 (STR-3) in human pancreatic cancer and pancreatic Carcinoma Cell lines and to investigate their regulation by retinoids. Methods—STR-3 expression was examined by immunohistochemistry in 21 human pancreatic Carcinomas. Expression of STR-3 and regulation by retinoids was assessed in five human pancreatic Carcinoma Cell lines using western and northern blotting as well as nuclear run on assays. Results—There was pronounced overexpression of STR-3 in 17 of 21 (80.9%) pancreatic Carcinoma specimens. STR-3 expression was predominantly located in peritumourous stromal Cells. Six of 21 (28.5%) Carcinomas also revealed STR-3 expression in epithelial tumour Cells whereas no STR-3 expression was observed in non-transformed pancreas. All five pancreatic Carcinoma Cell lines expressed STR-3 mRNA and protein. Furthermore, retinoid treatment results in a time and dose dependent inhibition of STR-3 protein expression. This inhibition seems to be post-transcriptional as neither STR-3 gene transcription nor mRNA steady state concentrations were affected by retinoids. Conclusions—STR-3 overexpression in stromal as well as epithelial elements during pancreatic carcinogenesis might contribute to the aggressive local growth and metastasis of pancreatic cancer and can be therapeutically targeted by retinoids. Keywords: matrix metalloproteinases; pancreatic cancer; stromelysin 3; retinoic acid