The Role of Protein Tyrosine Phosphatase Gamma in Human Breast Carcinogenesis PDF Download
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Author: Sherry T. Shu
Publisher:
ISBN:
Category : Carcinogenesis
Languages : en
Pages : 154
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Abstract: Reduced expression of protein tyrosine phosphatase gamma (PTPG) has been shown in breast cancer cell lines and cancerous tissue. PTPG over-expression in breast cancer cell line MCF-7 leads to the inhibition of cell proliferation and anchorage- independent growth. To further investigate the anti-carcinogenic abilities of PTPG in vivo, athymic nude mice were implanted with MCF-7 cells, which were stably transfected with PTPG cDNA (M7-PTPG) or empty vectors (M7-PCR). Tumor formation was significantly lower at the M7-PTPG cells implanted sites (10%) compared to sites where M7-PCR cells were implanted (100%), indicating that tumor formation was inhibited by the effect of PTPG in vivo. To explore the signaling pathway that PTPG is involved, breast cancer-related signaling cDNA array assays were performed. Seventy genes showed at least a 1.5 fold of expression difference in M7-PTPG cells compared to M7- PCR cells. The increase of the levels of p21(cip) and p27(kip) in M7-PTPG cells was confirmed by Western blot analyses. M7-PTPG cells also showed delayed re-entry into the cell cycle after the cells were released from G0/G1 cell cycle arrest, accompanied by lower phosphorylation levels of ERK1/2, compared to the control cells. Moreover, there was an aberrant methylation pattern in the PTPG promoter region of the breast cancer cell lines and patient's cancerous tissue. PTPG expression in SkBr3 cells can be recovered by treating with deoxy-5-azacytidine (DAC) and trichostatin A (TSA). Our results indicate that PTPG inhibits breast tumor promotion in vivo, presumably through cell cycle arrest by the up-regulated p21(cip) and p27(kip) proteins; and DNA methylation is a possible mechanism that leads to PTPG silencing in breast cancer cells. The results obtained from this study suggest that PTPG plays important role in breast carcinogenesis and may serve as a breast cancer therapeutic target.
Author: Sherry T. Shu
Publisher:
ISBN:
Category : Carcinogenesis
Languages : en
Pages : 154
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Book Description
Abstract: Reduced expression of protein tyrosine phosphatase gamma (PTPG) has been shown in breast cancer cell lines and cancerous tissue. PTPG over-expression in breast cancer cell line MCF-7 leads to the inhibition of cell proliferation and anchorage- independent growth. To further investigate the anti-carcinogenic abilities of PTPG in vivo, athymic nude mice were implanted with MCF-7 cells, which were stably transfected with PTPG cDNA (M7-PTPG) or empty vectors (M7-PCR). Tumor formation was significantly lower at the M7-PTPG cells implanted sites (10%) compared to sites where M7-PCR cells were implanted (100%), indicating that tumor formation was inhibited by the effect of PTPG in vivo. To explore the signaling pathway that PTPG is involved, breast cancer-related signaling cDNA array assays were performed. Seventy genes showed at least a 1.5 fold of expression difference in M7-PTPG cells compared to M7- PCR cells. The increase of the levels of p21(cip) and p27(kip) in M7-PTPG cells was confirmed by Western blot analyses. M7-PTPG cells also showed delayed re-entry into the cell cycle after the cells were released from G0/G1 cell cycle arrest, accompanied by lower phosphorylation levels of ERK1/2, compared to the control cells. Moreover, there was an aberrant methylation pattern in the PTPG promoter region of the breast cancer cell lines and patient's cancerous tissue. PTPG expression in SkBr3 cells can be recovered by treating with deoxy-5-azacytidine (DAC) and trichostatin A (TSA). Our results indicate that PTPG inhibits breast tumor promotion in vivo, presumably through cell cycle arrest by the up-regulated p21(cip) and p27(kip) proteins; and DNA methylation is a possible mechanism that leads to PTPG silencing in breast cancer cells. The results obtained from this study suggest that PTPG plays important role in breast carcinogenesis and may serve as a breast cancer therapeutic target.
Author: Yifan Zhai
Publisher:
ISBN:
Category : Breast
Languages : en
Pages : 296
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Book Description
![Modulation of Protein Tyrosine Phosphatase (PTP[gamma] Signaling by MicroRNA and Ligand Binding PDF](https://books.google.com/books/content/images/frontcover/Izg-nQAACAAJ?fife=w80-h100)
Author: Shu-Hong Lin
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Abstract: Protein Tyrosine Phosphatase [gamma] (PTP[gamma], encoded by PTPRG gene) has been shown to be an estrogen-regulated tumor suppressor in breast cancers. Our current studies focus on mechanisms which are influential in PTP[gamma] in both breast cancer cell line and primary cultured breast cancer cells. In search for the differences in micorRNA (miRNA) profiles among primary cultured human breast cancer cell (CEC) and adjacent normal cell (NAE), we found 24 up-regulated and 1 down-regulated miRNA in CEC. Among the up-regulated miRNAs, miR-141 is predicted to target PTPRG based on sequence and transient transfection of the precursor for miR-141 (pre-miR-141) in triple negative human breast cancer cell line, MDA-MB-231 cells successfully resulted in the down-regulation of PTPRG. Further experiments with 14 pairs of CEC and NAE from patients revealed a moderate negative association (Kendall's [tau] = -0.61) in NAE but not CEC. PTP[gamma] belongs to the receptor type phosphatase family, yet its ligand has not been reported until 2010. Members of contactin (CNTN) family, including CNTN3, 4, 5 and 6, were found to bind PTP[gamma]. However, it is still unclear whether CNTN binding is stimulatory or inhibitory to PTP[gamma] activity. Among the four possible ligands, only CNTN3 was found to be present in normal breast cells. In order to evaluate the impact of CNTN3 binding on PTP[gamma] signaling, we used genes regulated by PTP[gamma] as an indicator. Compared with PTPRG expression level, CNTN3/PTPRG ratio has been found to be equally and even better associated with the expression of downstream genes in CEC and NAE in an opposite direction. Such difference in the direction of association has suggested an inhibitory role for CNTN3 binding in terms of PTP[gamma] signaling.
Author:
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Category :
Languages : en
Pages :
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The folder may include clippings, announcements, small exhibition catalogs, and other ephemeral items.
Author: Christina Holzer
Publisher:
ISBN:
Category :
Languages : en
Pages : 80
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Author: Jun Zheng
Publisher:
ISBN:
Category :
Languages : en
Pages : 330
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Author: Universitat de València. Facultat de Ciències Biològiques
Publisher:
ISBN:
Category :
Languages : en
Pages : 158
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Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 33
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The aim of the studies covered under this report was to start addressing the potential role of protein tyrosine phosphatases in mammary tumorigenesis. On theoretical grounds, this class of enzymes could be expected to either act as negative regulators of growth (e.g. tumor suppressors), or to act oncogenically, e.g. by their ability to activate kinases that are negatively regulated by phosphorylation. We have addressed this question using RPTPa as a model PTP. Expression of this PTP has been surveyed in human breast cancers, in vitro studies have been performed to assess the effect of this PTP on growth properties and tumorigenicity of mammary carcinoma cells. Both approaches have led to the conclusion that increased expression of this PTP correlates with a less advanced stage of tumor progression. A number of studies have also been started to address the effect of RPTPa mouse gene ablation on models of mouse mammary tumorigenesis. These results suggest RPTPa may be useful as a marker for tumor progression, and raise a cautionary note regarding the use of PTP inhibitors in tumor therapy. These studies have been delayed with respect to the original timetable, but are proceeding. ------
Author: Benjamin G. Neel
Publisher: Springer
ISBN: 9781493981069
Category : Medical
Languages : en
Pages : 360
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This book aims to bridge the gap in understanding how protein-tyrosine phosphatases (PTPs), which carry out the reverse reaction of tyrosine phosphorylation, feature in cancer cell biology. The expertly authored chapters will first review the general features of the PTP superfamily, including their overall structure and enzymological properties; use selected examples of individual PTP superfamily members, to illustrate emerging data on the role of PTPs in cancer; and will review the current status of PTP-based drug development efforts. Protein Tyrosine Phosphatases in Cancer,from renowned researchers Benjamin Neel and Nicholas Tonks, is invaluable reading for researchers in oncology, stem cell signaling,and biochemistry.
Author: Cynthia Veenstra
Publisher:
ISBN: 9789176856031
Category :
Languages : en
Pages : 90
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