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Your search keyword '"Zang, Xiao-Ping"' showing total 3 results
Start Over Author "Zang, Xiao-Ping" Topic antineoplastic agents
3 results on '"Zang, Xiao-Ping"'

1. Selective growth inhibition of cancer cells by L-methioninase-containing fusion protein targeted to the urokinase receptor.

Author

Palwai NR, Zang XP, Harrison RG, Benbrook D, and Pento JT

Subjects
Cell Line, Tumor, Cell Movement drug effects, Cell Survival drug effects, Dose-Response Relationship, Drug, Drug Delivery Systems, Humans, Mutation, Recombinant Fusion Proteins genetics, Antineoplastic Agents pharmacology, Carbon-Sulfur Lyases genetics, Cell Proliferation drug effects, Receptors, Urokinase Plasminogen Activator metabolism, Recombinant Fusion Proteins pharmacology
Abstract

Background: We have reported the development of a novel fusion protein (FP) consisting of an amino-terminal fragment of urokinase linked to the amino terminus of the enzyme L-methioninase (L-M). The present study compared the effect of this novel FP on the proliferation of human ovarian, skin, breast endometrial and pancreatic cancer cell lines., Methods: The FP, L-M and a mutated FP, with reduced L-M activity, were produced by recombinant methods. The effect of treatment with FP, L-M and mutated FP on the proliferation of the cancer cells was measured in vitro using an MTS assay., Results: The inhibitory effect of the FP was found to be significantly greater than that of L-M alone or the mutated FP. In addition, the FP produced a greater inhibitory effect on an ovarian cancer cell line than on comparable normal, non-cancerous cells. Further, the FP produced a dose-dependent inhibition of the proliferation of pancreatic cancer cell lines., Conclusion: These results suggest that this FP is a potent and selective inhibitor of the proliferation of various cancer cell lines and has potential as a therapeutic agent for the treatment of various methionine-dependent cancers., (Copyright 2009 S. Karger AG, Basel.)

Published
2009
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2. The effect of antiestrogens on TGF-beta-mediated chemotaxis of human breast cancer cells.

Author

Tong GM, Rajah TT, Zang XP, and Pento JT

Subjects
Breast Neoplasms drug therapy, Collagenases metabolism, Estradiol pharmacology, Fulvestrant, Humans, Receptors, Transforming Growth Factor beta biosynthesis, Tamoxifen pharmacology, Transforming Growth Factor beta pharmacology, Tumor Cells, Cultured, Antineoplastic Agents pharmacology, Breast Neoplasms pathology, Chemotaxis drug effects, Estradiol analogs & derivatives, Estrogen Receptor Modulators pharmacology, Tamoxifen analogs & derivatives, Transforming Growth Factor beta antagonists & inhibitors
Abstract

Background: In a previous study we compared the influence of several growth factors on cancer cells in culture and observed that transforming growth factor-beta (TGF-beta) enhanced the invasiveness of several breast cancer cell lines. The objective of the present study was to determine the influence of three unique antiestrogens on TGF-beta-mediated chemotaxis of human breast cancer cells., Materials and Methods: The chemotactic activity of TGF-beta was assayed in vitro using collagen IV-coated transwell chambers with either MCF-7 or MDA-MB-231 human breast cancer cells. The cells were pretreated with antiestrogen for 4 days, harvested and placed in the upper transwell chamber. TGF-beta was added to the lower chamber and cell migration and collagenase release were determined following a 6-hour incubation., Results: In this study TGF-beta enhanced the chemotaxis of both cell types with a much greater effect on the MDA-MB-231 cells. However, TGF-beta-mediated chemotaxis of the MCF-7 cells was inhibited by antiestrogen pretreatment while TGF-beta-mediated chemotaxis of the MDA-MB-231 cells was not altered. Further, neither TGF-beta nor antiestrogen treatment altered collagenase release from either cell line., Conclusion: The data demonstrate that pure antiestrogens are capable of inhibiting TGF-beta-mediated chemotaxis in estrogen receptor (ER)-positive breast cancer cells by a mechanism which is independent of collagenase release. Finally, the results of this study suggest a coupling of the TGF-beta and ER signaling pathways and indicate that TGF-beta may be an important therapeutic target for the treatment or inhibition of breast cancer metastasis.

Published
2002

3. Selective Growth Inhibition of Cancer Cells by L-Methioninase-Containing Fusion Protein Targeted to the Urokinase Receptor

Author

Palwai, Naveen R., Zang, Xiao-Ping, Harrison, Roger G., Benbrook, Doris, and Pento, J. Thomas

Subjects
Carbon-Sulfur Lyases, Drug Delivery Systems, Dose-Response Relationship, Drug, Cell Movement, Cell Survival, Short Communication, Cell Line, Tumor, Recombinant Fusion Proteins, Mutation, Humans, Antineoplastic Agents, Cell Proliferation, Receptors, Urokinase Plasminogen Activator
Abstract

We have reported the development of a novel fusion protein (FP) consisting of an amino-terminal fragment of urokinase linked to the amino terminus of the enzyme L-methioninase (L-M). The present study compared the effect of this novel FP on the proliferation of human ovarian, skin, breast endometrial and pancreatic cancer cell lines.The FP, L-M and a mutated FP, with reduced L-M activity, were produced by recombinant methods. The effect of treatment with FP, L-M and mutated FP on the proliferation of the cancer cells was measured in vitro using an MTS assay.The inhibitory effect of the FP was found to be significantly greater than that of L-M alone or the mutated FP. In addition, the FP produced a greater inhibitory effect on an ovarian cancer cell line than on comparable normal, non-cancerous cells. Further, the FP produced a dose-dependent inhibition of the proliferation of pancreatic cancer cell lines.These results suggest that this FP is a potent and selective inhibitor of the proliferation of various cancer cell lines and has potential as a therapeutic agent for the treatment of various methionine-dependent cancers.

Published
2009

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