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The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform

Sylvia K Plevritis - One of the best experts on this subject based on the ideXlab platform.

  • mapping lung cancer epithelial mesenchymal transition states and trajectories with single cell resolution
    Nature Communications, 2019
    Co-Authors: Loukia G Karacosta, Benedict Anchang, Nikolaos Ignatiadis, Samuel C Kimmey, Jalen Benson, Joseph B Shrager, Robert Tibshirani, Sean C Bendall, Sylvia K Plevritis
    Abstract:

    Elucidating the spectrum of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states in clinical samples promises insights on cancer progression and drug resistance. Using mass cytometry time-course analysis, we resolve lung cancer EMT states through TGFβ-treatment and identify, through TGFβ-withdrawal, a distinct MET state. We demonstrate significant differences between EMT and MET trajectories using a computational tool (TRACER) for reconstructing trajectories between cell states. In addition, we construct a lung cancer reference map of EMT and MET states referred to as the EMT-MET PHENOtypic STAte MaP (PHENOSTAMP). Using a neural net algorithm, we project clinical samples onto the EMT-MET PHENOSTAMP to characterize their phenotypic profile with single-cell resolution in terms of our in vitro EMT-MET analysis. In summary, we provide a framework to phenotypically characterize clinical samples in the context of in vitro EMT-MET findings which could help assess clinical relevance of EMT in cancer in future studies. Intermediate transitions between epithelial and mesenchymal states are associated with tumor progression. Here using mass cytometry, Plevritis and colleagues develop a computational framework to resolve and map these trajectories in lung cancer cells and clinical specimens.

  • mapping lung cancer epithelial mesenchymal transition states and trajectories with single cell resolution
    bioRxiv, 2019
    Co-Authors: Loukia G Karacosta, Benedict Anchang, Nikolaos Ignatiadis, Samuel C Kimmey, Jalen Benson, Joseph B Shrager, Robert Tibshirani, Sean C Bendall, Sylvia K Plevritis
    Abstract:

    ABSTRACT Elucidating a continuum of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states in clinical samples promises new insights in cancer progression and drug response. Using mass cytometry time-course analysis, we resolve lung cancer EMT states through TGFβ-treatment and identify through TGFβ-withdrawal, an MET state previously unrealized. We demonstrate significant differences between EMT and MET trajectories using a novel computational tool (TRACER) for reconstructing trajectories between cell states. Additionally, we construct a lung cancer reference map of EMT and MET states referred to as the EMT-MET STAte MaP (STAMP). Using a neural net algorithm, we project clinical samples onto the EMT-MET STAMP to characterize their phenotypic profile with single-cell resolution in terms of our in vitro EMT-MET analysis. In summary, we provide a framework that can be extended to phenotypically characterize clinical samples in the context of in vitro studies showing differential EMT-MET traits related to metastasis and drug sensitivity.

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

  • MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model
    Elsevier, 2019
    Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin Tian
    Abstract:

    Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis. Keywords: microRNA-29b, mesenchymal-epithelial transition, silicosis, epithelial-mesenchymal transition, lung functio

  • MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
    Molecular therapy. Nucleic acids, 2018
    Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin Tian
    Abstract:

    Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.

John T Powers - One of the best experts on this subject based on the ideXlab platform.

  • the epithelial mesenchymal transition factor snail paradoxically enhances reprogramming
    Stem cell reports, 2014
    Co-Authors: Juli Unternaehrer, Rui Zhao, Kitai Kim, Marcella Cesana, John T Powers
    Abstract:

    Reprogramming of fibroblasts to induced pluripotent stem cells (iPSCs) entails a mesenchymal to epithelial transition (MET). While attempting to dissect the mechanism of MET during reprogramming, we observed that knockdown (KD) of the epithelial-to-mesenchymal transition (EMT) factor SNAI1 (SNAIL) paradoxically reduced, while overexpression enhanced, reprogramming efficiency in human cells and in mouse cells, depending on strain. We observed nuclear localization of SNAI1 at an early stage of fibroblast reprogramming and using mouse fibroblasts expressing a knockin SNAI1-YFP reporter found cells expressing SNAI1 reprogrammed at higher efficiency. We further demonstrated that SNAI1 binds the let-7 promoter, which may play a role in reduced expression of let-7 microRNAs, enforced expression of which, early in the reprogramming process, compromises efficiency. Our data reveal an unexpected role for the EMT factor SNAI1 in reprogramming somatic cells to pluripotency.

Loukia G Karacosta - One of the best experts on this subject based on the ideXlab platform.

  • mapping lung cancer epithelial mesenchymal transition states and trajectories with single cell resolution
    Nature Communications, 2019
    Co-Authors: Loukia G Karacosta, Benedict Anchang, Nikolaos Ignatiadis, Samuel C Kimmey, Jalen Benson, Joseph B Shrager, Robert Tibshirani, Sean C Bendall, Sylvia K Plevritis
    Abstract:

    Elucidating the spectrum of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states in clinical samples promises insights on cancer progression and drug resistance. Using mass cytometry time-course analysis, we resolve lung cancer EMT states through TGFβ-treatment and identify, through TGFβ-withdrawal, a distinct MET state. We demonstrate significant differences between EMT and MET trajectories using a computational tool (TRACER) for reconstructing trajectories between cell states. In addition, we construct a lung cancer reference map of EMT and MET states referred to as the EMT-MET PHENOtypic STAte MaP (PHENOSTAMP). Using a neural net algorithm, we project clinical samples onto the EMT-MET PHENOSTAMP to characterize their phenotypic profile with single-cell resolution in terms of our in vitro EMT-MET analysis. In summary, we provide a framework to phenotypically characterize clinical samples in the context of in vitro EMT-MET findings which could help assess clinical relevance of EMT in cancer in future studies. Intermediate transitions between epithelial and mesenchymal states are associated with tumor progression. Here using mass cytometry, Plevritis and colleagues develop a computational framework to resolve and map these trajectories in lung cancer cells and clinical specimens.

  • mapping lung cancer epithelial mesenchymal transition states and trajectories with single cell resolution
    bioRxiv, 2019
    Co-Authors: Loukia G Karacosta, Benedict Anchang, Nikolaos Ignatiadis, Samuel C Kimmey, Jalen Benson, Joseph B Shrager, Robert Tibshirani, Sean C Bendall, Sylvia K Plevritis
    Abstract:

    ABSTRACT Elucidating a continuum of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states in clinical samples promises new insights in cancer progression and drug response. Using mass cytometry time-course analysis, we resolve lung cancer EMT states through TGFβ-treatment and identify through TGFβ-withdrawal, an MET state previously unrealized. We demonstrate significant differences between EMT and MET trajectories using a novel computational tool (TRACER) for reconstructing trajectories between cell states. Additionally, we construct a lung cancer reference map of EMT and MET states referred to as the EMT-MET STAte MaP (STAMP). Using a neural net algorithm, we project clinical samples onto the EMT-MET STAMP to characterize their phenotypic profile with single-cell resolution in terms of our in vitro EMT-MET analysis. In summary, we provide a framework that can be extended to phenotypically characterize clinical samples in the context of in vitro studies showing differential EMT-MET traits related to metastasis and drug sensitivity.

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

  • MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model
    Elsevier, 2019
    Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin Tian
    Abstract:

    Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis. Keywords: microRNA-29b, mesenchymal-epithelial transition, silicosis, epithelial-mesenchymal transition, lung functio

  • MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model.
    Molecular therapy. Nucleic acids, 2018
    Co-Authors: Jingping Sun, Ximeng Lian, Zhonghui Zhu, Xiaowei Chen, Wanying Pei, Ali Abbas, Yan Wang, Lin Tian
    Abstract:

    Lung epithelial-mesenchymal transition (EMT) plays an important role in silicosis fibrosis. The reverse process of EMT is mesenchymal-epithelial transition (MET), which is viewed as an anti-EMT therapy and is a good target toward fibrosis. MicroRNAs (miRNAs) have emerged as potent regulators of EMT and MET programs, and, hence, we tested the miRNA expression using microarray assay and investigated their roles in silica-induced EMT in lung epithelial cells. We found that miRNA-29b (miR-29b) was dynamically downregulated by silica and influenced the promotion of MET in RLE-6TN cells. Furthermore, delivery of miR-29b to mice significantly inhibited silica-induced EMT, prevented lung fibrosis, and improved lung function. Together, our results clearly demonstrated that miR-29b acted as a novel negative regulator of silicosis fibrosis-inhibited lung fibrosis, probably by promoting MET and by suppressing EMT in the lung. These findings may represent a new potential therapeutic target for treating silicosis fibrosis.