The Experts below are selected from a list of 42 Experts worldwide ranked by ideXlab platform

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

  • The Homeotic Protein Six3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

  • the homeotic protein Six3 suppresses carcinogenesis and metastasis through recruiting the lsd1 nurd mta3 complex
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang, Yan Wang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

Yves Labelle - One of the best experts on this subject based on the ideXlab platform.

  • functional characterization of Six3 homeodomain mutations in holoprosencephaly interaction with the nuclear receptor nr4a3 nor1
    Human Mutation, 2004
    Co-Authors: Cynthia Laflamme, Christine Filion, Yves Labelle
    Abstract:

    Holoprosencephaly (HPE) is a relatively common brain malformation resulting in an incomplete separation of the two cerebral hemispheres. A number of mutations in different genes have been linked to this malformation, including three missense mutations in the homeodomain of the Transcription Factor Six3. In this study, we investigated the functional consequences of these Six3 mutations with respect to the ability of the protein to interact with and stimulate the Transcriptional activity of the nuclear receptor NOR1 (NR4A3). Using glutathione S-transferase fusion protein pull-down assays and transient cotransfections of Neuro-2a cells with expression and reporter vectors, we found that one mutation, c.676C>G (p.L226V), does not alter the properties of Six3 toward NOR1. Another mutation, c.749T>C (p.V250A), results in the production of a highly unstable protein in Neuro-2a cells. The third mutation, c.770G>C (p.R257P), results in a mutant Six3 protein that no longer interacts with NOR1 in vivo. These observations suggest that different Six3 mutations in HPE2 may affect different signaling pathways, and that one of these pathways may involve the nuclear receptor NOR1. Hum Mutat 24:502–508, 2004. © 2004 Wiley-Liss, Inc.

  • Functional characterization of Six3 homeodomain mutations in holoprosencephaly: interaction with the nuclear receptor NR4A3/NOR1.
    Human Mutation, 2004
    Co-Authors: Cynthia Laflamme, Christine Filion, Yves Labelle
    Abstract:

    Holoprosencephaly (HPE) is a relatively common brain malformation resulting in an incomplete separation of the two cerebral hemispheres. A number of mutations in different genes have been linked to this malformation, including three missense mutations in the homeodomain of the Transcription Factor Six3. In this study, we investigated the functional consequences of these Six3 mutations with respect to the ability of the protein to interact with and stimulate the Transcriptional activity of the nuclear receptor NOR1 (NR4A3). Using glutathione S-transferase fusion protein pull-down assays and transient cotransfections of Neuro-2a cells with expression and reporter vectors, we found that one mutation, c.676C>G (p.L226V), does not alter the properties of Six3 toward NOR1. Another mutation, c.749T>C (p.V250A), results in the production of a highly unstable protein in Neuro-2a cells. The third mutation, c.770G>C (p.R257P), results in a mutant Six3 protein that no longer interacts with NOR1 in vivo. These observations suggest that different Six3 mutations in HPE2 may affect different signaling pathways, and that one of these pathways may involve the nuclear receptor NOR1. Hum Mutat 24:502–508, 2004. © 2004 Wiley-Liss, Inc.

Yu Zheng - One of the best experts on this subject based on the ideXlab platform.

  • The Homeotic Protein Six3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

  • the homeotic protein Six3 suppresses carcinogenesis and metastasis through recruiting the lsd1 nurd mta3 complex
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang, Yan Wang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

Yan Wang - One of the best experts on this subject based on the ideXlab platform.

  • the homeotic protein Six3 suppresses carcinogenesis and metastasis through recruiting the lsd1 nurd mta3 complex
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang, Yan Wang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

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

  • The Homeotic Protein Six3 Suppresses Carcinogenesis and Metastasis through Recruiting the LSD1/NuRD(MTA3) Complex.
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.

  • the homeotic protein Six3 suppresses carcinogenesis and metastasis through recruiting the lsd1 nurd mta3 complex
    Theranostics, 2018
    Co-Authors: Yu Zheng, Shuai Leng, Dandan Feng, Yi Zeng, Wei Huang, Shuang Wang, Yang Yang, Yan Wang
    Abstract:

    : The homeodomain Transcription Factor Six3 was recently reported to be a negative regulator of the Wnt pathway and has an emerging role in cancer. However, how Six3 contributes to tumorigenesis and metastasis is poorly understood. METHODS: We employed affinity purification and mass spectrometry (MS) to identify the proteins physically associated with Six3. Genome-wide analysis of the Six3/LSD1/NuRD(MTA3) complex using a chromatin immunoprecipitation-on-chip approach identified a cohort of target genes including WNT1 and FOXC2, which are critically involved in cell proliferation and epithelial-to-mesenchymal transition. Also, we used flow cytometry, growth curve analysis, EdU incorporation assay, colony formation assays, trans-well invasion assays, immunohistochemical staining and in vivo bioluminescence assay to investigate the function of Six3 in tumorigenesis. RESULTS: We demonstrate that the Six3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer. Six3 expression is downregulated in various human cancers and high Six3 is correlated with improved prognosis. CONCLUSION: Our study revealed an important mechanistic link between the loss of function of Six3 and tumor progression, identified a molecular basis for the opposing actions of MTA1 and MTA3, and may provide new potential prognostic indicators and targets for cancer therapy.