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Hengphon Too - One of the best experts on this subject based on the ideXlab platform.

  • a specific isoform of Glial Cell Line derived neurotrophic factor family receptor alpha 1 regulates rhoa expression and glioma Cell migration
    Journal of Neurochemistry, 2010
    Co-Authors: Guoqiang Wan, Hengphon Too
    Abstract:

    J. Neurochem. (2010) 115, 759–770. Abstract Malignant gliomas are highly invasive neuroepithelial tumors where the tendency to invade and migrate away from the primary tumor mass is thought to be a leading cause of tumor recurrence and treatment failures. Autocrine signals produced by secreted factors that signal through receptors on the tumor are known to contribute to the invasiveness. Glial Cell Line-derived neurotrophic factor and GDNF family receptor alpha 1 (GFRα1) are over-expressed in human gliomas. We have previously reported that human gliomas express high levels of GFRα1b, an alternatively spliced isoform of GFRα1. However, the functional significance of GFRα1b in glioma behaviors is currently unknown. In this study, we have designed isoform-specific small-interfering RNA to knockdown the highly homologous GFRα1a or GFRα1b isoform efficiently in malignant C6 glioma Cells. Unexpectedly, the knockdown of GFRα1b but not GFRα1a induced Cell elongation and inhibited C6 Cell migration and invasion in vitro. In addition, GFRα1b was found to regulate the expression of RhoA small GTPase, which was required for migration of C6 Cells. The decreases in RhoA expression and Cell migration after GFRα1b knockdown were attenuated by small-interfering RNA -resistant GFRα1b but not GFRα1a, further demonstrating the specific role of GFRα1b in glioma migration. Interestingly, the knockdown of NCAM but not receptor tyrosine kinase Ret resulted in the reduction of RhoA expression and C6 Cell migration. Taken together, these unanticipated results indicate that GFRα1b is involved in glioma migration through Glial Cell Line-derived neurotrophic factor –GFRα1b-NCAM signaling complex and modulation of RhoA expression.

Michael S Goligorsky - One of the best experts on this subject based on the ideXlab platform.

Yi Dai - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of trpa1 channel activity in sensory neurons by the Glial Cell Line derived neurotrophic factor family member artemin
    Molecular Pain, 2011
    Co-Authors: Naoki Yoshida, Kimiko Kobayashi, Shenglan Wang, Satoshi Yamamoto, Koichi Noguchi, Yi Dai
    Abstract:

    Background The transient receptor potential (TRP) channel subtype A1 (TRPA1) is known to be expressed on sensory neurons and respond to changes in temperature, pH and local application of certain noxious chemicals such as allyl isothiocyanate (AITC). Artemin is a neuronal survival and differentiation factor and belongs to the Glial Cell Line-derived neurotrophic factor (GDNF) family. Both TRPA1 and artemin have been reported to be involved in pathological pain initiation and maintenance. In the present study, using whole-Cell patch clamp recording technique, in situ hybridization and behavioral analyses, we examined the functional interaction between TRPA1 and artemin.

Guoqiang Wan - One of the best experts on this subject based on the ideXlab platform.

  • a specific isoform of Glial Cell Line derived neurotrophic factor family receptor alpha 1 regulates rhoa expression and glioma Cell migration
    Journal of Neurochemistry, 2010
    Co-Authors: Guoqiang Wan, Hengphon Too
    Abstract:

    J. Neurochem. (2010) 115, 759–770. Abstract Malignant gliomas are highly invasive neuroepithelial tumors where the tendency to invade and migrate away from the primary tumor mass is thought to be a leading cause of tumor recurrence and treatment failures. Autocrine signals produced by secreted factors that signal through receptors on the tumor are known to contribute to the invasiveness. Glial Cell Line-derived neurotrophic factor and GDNF family receptor alpha 1 (GFRα1) are over-expressed in human gliomas. We have previously reported that human gliomas express high levels of GFRα1b, an alternatively spliced isoform of GFRα1. However, the functional significance of GFRα1b in glioma behaviors is currently unknown. In this study, we have designed isoform-specific small-interfering RNA to knockdown the highly homologous GFRα1a or GFRα1b isoform efficiently in malignant C6 glioma Cells. Unexpectedly, the knockdown of GFRα1b but not GFRα1a induced Cell elongation and inhibited C6 Cell migration and invasion in vitro. In addition, GFRα1b was found to regulate the expression of RhoA small GTPase, which was required for migration of C6 Cells. The decreases in RhoA expression and Cell migration after GFRα1b knockdown were attenuated by small-interfering RNA -resistant GFRα1b but not GFRα1a, further demonstrating the specific role of GFRα1b in glioma migration. Interestingly, the knockdown of NCAM but not receptor tyrosine kinase Ret resulted in the reduction of RhoA expression and C6 Cell migration. Taken together, these unanticipated results indicate that GFRα1b is involved in glioma migration through Glial Cell Line-derived neurotrophic factor –GFRα1b-NCAM signaling complex and modulation of RhoA expression.

Haikun Shi - One of the best experts on this subject based on the ideXlab platform.