The Experts below are selected from a list of 4821 Experts worldwide ranked by ideXlab platform

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

  • MALAT1 regulates serum response factor through miR-133 as a competing endogenous RNA in myogenesis
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015
    Co-Authors: Xiaorui Han, Feng Yang, Huiqing Cao, Zicai Liang
    Abstract:

    Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an example of a functional long noncoding RNA involved in many biologic processes. However, the mechanisms for MALAT1 in myogenesis are unclear. Serum response factor (SRF) is a pivotal transcription factor for muscle proliferation and differentiation and is reported to be a target gene for muscle-specific microRNA-133 (miR-133). In this study, we initially found that silencing MALAT1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased MALAT1 expression as well. Further study revealed that MALAT1 contained an miR-133 functional target site, and the interplay between MALAT1 and Srf was miR-133 dependent. We demonstrated that MALAT1 modulates Srf through miR-133 as a competing endogenous RNA and established a novel connection among MALAT1, miR-133, and Srf in myoblast differentiation.

  • MALAT1 regulates serum response factor through mir 133 as a competing endogenous rna in myogenesis
    The FASEB Journal, 2015
    Co-Authors: Feng Yang, Zicai Liang
    Abstract:

    Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an example of a functional long noncoding RNA involved in many biologic processes. However, the mechanisms for MALAT1 in myogenesis are unclear. Serum response factor (SRF) is a pivotal transcription factor for muscle proliferation and differentiation and is reported to be a target gene for muscle-specific microRNA-133 (miR-133). In this study, we initially found that silencing MALAT1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased MALAT1 expression as well. Further study revealed that MALAT1 contained an miR-133 functional target site, and the interplay between MALAT1 and Srf was miR-133 dependent. We demonstrated that MALAT1 modulates Srf through miR-133 as a competing endogenous RNA and established a novel connection among MALAT1, miR-133, and Srf in myoblast differentiation.—Han, X., Yang, F., Cao, H., Liang. Z. MALAT1 regulates serum ...

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

  • MALAT1 induces tongue cancer cells emt and inhibits apoptosis through wnt β catenin signaling pathway
    Journal of Oral Pathology & Medicine, 2017
    Co-Authors: Jun Liang, Lizhong Liang, Kexiong Ouyang
    Abstract:

    Background MALAT1 is recognized as an oncogenic lncRNA in various malignancies. However, its expression and function in oral tongue squamous cell carcinoma are still unknown. This study aims to investigate the expression and function of MALAT1 in TSCC tissues and cells. Materials and Methods qPCR was performed to detect the expression of MALAT1. MALAT1 was suppressed and upregulated by plasmid transfection in TSCC cells, and then cell migration, invasion, EMT, and apoptosis were analyzed. Results LncRNA MALAT1 was upregulated in TSCC tissues and correlated with cervical lymph node metastasis in TSCC patients. Moreover, MALAT1 induced cell migration, invasion, EMT, and inhibited apoptosis by modulating Wnt/β-catenin signaling pathway. Finally, inhibiting Wnt/β-catenin signaling pathway attenuated the effect of exogenous MALAT1. Conclusion In summary, upregulated MALAT1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β-catenin signaling pathway.

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

  • MALAT1 regulates serum response factor through miR-133 as a competing endogenous RNA in myogenesis
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015
    Co-Authors: Xiaorui Han, Feng Yang, Huiqing Cao, Zicai Liang
    Abstract:

    Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an example of a functional long noncoding RNA involved in many biologic processes. However, the mechanisms for MALAT1 in myogenesis are unclear. Serum response factor (SRF) is a pivotal transcription factor for muscle proliferation and differentiation and is reported to be a target gene for muscle-specific microRNA-133 (miR-133). In this study, we initially found that silencing MALAT1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased MALAT1 expression as well. Further study revealed that MALAT1 contained an miR-133 functional target site, and the interplay between MALAT1 and Srf was miR-133 dependent. We demonstrated that MALAT1 modulates Srf through miR-133 as a competing endogenous RNA and established a novel connection among MALAT1, miR-133, and Srf in myoblast differentiation.

  • MALAT1 regulates serum response factor through mir 133 as a competing endogenous rna in myogenesis
    The FASEB Journal, 2015
    Co-Authors: Feng Yang, Zicai Liang
    Abstract:

    Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an example of a functional long noncoding RNA involved in many biologic processes. However, the mechanisms for MALAT1 in myogenesis are unclear. Serum response factor (SRF) is a pivotal transcription factor for muscle proliferation and differentiation and is reported to be a target gene for muscle-specific microRNA-133 (miR-133). In this study, we initially found that silencing MALAT1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased MALAT1 expression as well. Further study revealed that MALAT1 contained an miR-133 functional target site, and the interplay between MALAT1 and Srf was miR-133 dependent. We demonstrated that MALAT1 modulates Srf through miR-133 as a competing endogenous RNA and established a novel connection among MALAT1, miR-133, and Srf in myoblast differentiation.—Han, X., Yang, F., Cao, H., Liang. Z. MALAT1 regulates serum ...

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

  • MALAT1 induces tongue cancer cells emt and inhibits apoptosis through wnt β catenin signaling pathway
    Journal of Oral Pathology & Medicine, 2017
    Co-Authors: Jun Liang, Lizhong Liang, Kexiong Ouyang
    Abstract:

    Background MALAT1 is recognized as an oncogenic lncRNA in various malignancies. However, its expression and function in oral tongue squamous cell carcinoma are still unknown. This study aims to investigate the expression and function of MALAT1 in TSCC tissues and cells. Materials and Methods qPCR was performed to detect the expression of MALAT1. MALAT1 was suppressed and upregulated by plasmid transfection in TSCC cells, and then cell migration, invasion, EMT, and apoptosis were analyzed. Results LncRNA MALAT1 was upregulated in TSCC tissues and correlated with cervical lymph node metastasis in TSCC patients. Moreover, MALAT1 induced cell migration, invasion, EMT, and inhibited apoptosis by modulating Wnt/β-catenin signaling pathway. Finally, inhibiting Wnt/β-catenin signaling pathway attenuated the effect of exogenous MALAT1. Conclusion In summary, upregulated MALAT1 in TSCC promoted EMT and inhibited cell apoptosis by modulating Wnt/β-catenin signaling pathway.

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

  • long non coding rna MALAT1 promotes proliferation and invasion via targeting mir 129 5p in triple negative breast cancer
    Biomedicine & Pharmacotherapy, 2017
    Co-Authors: Yonggang Zuo, Zhenyu Zhou
    Abstract:

    Abstract Background Long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) play important roles in tumor progression. In the present study, we determined the regulatory function of MALAT1 in triple-negative breast cancer (TNBC). Methods A total of 43 cases of TNBC tissues and paired adjacent non-tumor tissues were collected for the research. MALAT1 expression was explored by qRT-PCR. In vitro functional validation experiments were used to determine the effect of MALAT1 on TNBC progression. We further identified the downstream target miRNAs for MALAT1. Results Relative expression of MALAT1 was increased in TNBC tissues and cell lines. High MALAT1 expression was closely correlated to advance clinical features and poor overall survival in TNBC patients. Function assay showed that MALAT1 silencing significantly decreased cell proliferation, migration, and invasion. Flow cytometry assay revealed that MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. In addition, we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p. Conclusion Our results demonstrated that the “MALAT1-miR-129-5p” axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC.