Literature DB >> 32135188

Non-coding RNAs and nuclear architecture during epithelial-mesenchymal transition in lung cancer and idiopathic pulmonary fibrosis.

Karla Rubio1, Rafael Castillo-Negrete1, Guillermo Barreto2.   

Abstract

Lung cancer (LC) is the leading cause of cancer-related deaths worldwide. On the other hand, idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease showing a prevalence of 20 new cases per 100,000 persons per year. Despite differences in cellular origin and pathological phenotypes, LC and IPF are lung diseases that share common features, including hyperproliferation of specific cell types in the lung, involvement of epithelial-mesenchymal transition (EMT) and enhanced activity of signaling pathways, such as tissue growth factor (TGFB), epidermal growth factor (EGF), fibroblast growth factor (FGF), wingless secreted glycoprotein (WNT) signaling, among others. EMT is a process during which epithelial cells lose their cell polarity and cell-cell adhesion, and acquire migratory and invasive properties to become mesenchymal cells. EMT involves numerous morphological hallmarks of hyperproliferative diseases, like cell plasticity, resistance to apoptosis, dedifferentiation and proliferation, thereby playing a central role during organ fibrosis and cancer progression. EMT was considered as an "all-or-none" process. In contrast to these outdated dichotomist interpretations, recent reports suggest that EMT occurs gradually involving different epithelial cell intermediate states with mesenchyme-like characteristics. These cell intermediate states of EMT differ from each other in their cell plasticity, invasiveness and metastatic potential, which in turn are induced by signals from their microenvironment. EMT is regulated by several transcription factors (TFs), which are members of prominent families of master regulators of transcription. In addition, there is increasing evidence for the important contribution of noncoding RNAs (ncRNAs) to EMT. In our review we highlight articles dissecting the function of different ncRNAs subtypes and nuclear architecture in cell intermediate states of EMT, as well as their involvement in LC and IPF.
Copyright © 2020 Elsevier Inc. All rights reserved.

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Year:  2020        PMID: 32135188     DOI: 10.1016/j.cellsig.2020.109593

Source DB:  PubMed          Journal:  Cell Signal        ISSN: 0898-6568            Impact factor:   4.315


  5 in total

1.  The molecular mechanism of Ligusticum wallichii for improving idiopathic pulmonary fibrosis: A network pharmacology and molecular docking study.

Authors:  Xiaozheng Wu; Wen Li; Zhenliang Luo; Yunzhi Chen
Journal:  Medicine (Baltimore)       Date:  2022-02-11       Impact factor: 1.817

Review 2.  Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.

Authors:  Miguel Ángel Olmedo-Suárez; Ivonne Ramírez-Díaz; Andrea Pérez-González; Alejandro Molina-Herrera; Miguel Ángel Coral-García; Sagrario Lobato; Pouya Sarvari; Guillermo Barreto; Karla Rubio
Journal:  Biomolecules       Date:  2022-03-28

3.  Diagnostic Value of Serum Levels of IL-22, IL-23, and IL-17 for Idiopathic Pulmonary Fibrosis Associated with Lung Cancer.

Authors:  Qian Zhang; Lihong Tong; Bing Wang; Ting Wang; Hongxia Ma
Journal:  Ther Clin Risk Manag       Date:  2022-04-19       Impact factor: 2.755

4.  ADAR1 Isoforms Regulate Let-7d Processing in Idiopathic Pulmonary Fibrosis.

Authors:  Gabriela Díaz-Piña; Karla Rubio; Rosa M Ordoñez-Razo; Guillermo Barreto; Eduardo Montes; Carina Becerril; Alfonso Salgado; Héctor Cabrera-Fuentes; Arnoldo Aquino-Galvez; Angeles Carlos-Reyes; Victor Ruiz
Journal:  Int J Mol Sci       Date:  2022-08-12       Impact factor: 6.208

Review 5.  Pathophysiological Roles of Stress-Activated Protein Kinases in Pulmonary Fibrosis.

Authors:  Yoshitoshi Kasuya; Jun-Dal Kim; Masahiko Hatano; Koichiro Tatsumi; Shuichi Matsuda
Journal:  Int J Mol Sci       Date:  2021-06-03       Impact factor: 5.923

  5 in total

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