Long Noncoding RNA MALAT1 Promotes Laryngocarcinoma Development by Targeting miR-708-5p/BRD4 Axis to Regulate YAP1-Mediated Epithelial-Mesenchymal Transition.

Objective. The objective of this study was to investigate whether long noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) contributes to laryngocarcinoma development via regulating the Yes-associated protein 1- (YAP1-) mediated epithelial-mesenchymal transition (EMT) and t...

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Published in:BioMed Research International pp. 1 - 12
Main Authors: Wu, Xiaoqin, Tan, Yenong, Tang, Xuxia
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell 5/12/2022
Online Access:View this record in EBSCOhost
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      dt: 5/12/2022
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        156849837
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        10.1155/2022/8093949
        156849837
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        atl: Long Noncoding RNA MALAT1 Promotes Laryngocarcinoma Development by Targeting miR-708-5p/BRD4 Axis to Regulate YAP1-Mediated Epithelial-Mesenchymal Transition.
      aug:
        au:
          Wu, Xiaoqin
          Tan, Yenong
          Tang, Xuxia
        affil: Department of Otolaryngology, Hainan Provincial Hospital of Traditional Chinese Medicine, Haikou, Hainan, China
      sug:
        subj:
          RNA Physiology
          Laryngeal Neoplasms Risk Factors
          YAP-Signaling Proteins Metabolism
          Epithelial-Mesenchymal Transition
          MicroRNA
          Adenocarcinoma of Lung Complications
          Neoplasm Metastasis Complications
          Risk Assessment
          Human
          Phenotype
          In Vitro Studies
          In Vivo Studies
          Cell Line, Tumor
          Cell Proliferation
          Apoptosis
          Cell Movement
          Bromodomain Containing Proteins
      ab: Objective. The objective of this study was to investigate whether long noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) contributes to laryngocarcinoma development via regulating the Yes-associated protein 1- (YAP1-) mediated epithelial-mesenchymal transition (EMT) and the underlying mechanism. Methods. The effects of MALAT1 suppression and BET inhibitor JQ1 on the malignant phenotypes and cancer stem cell- (CSC-) like properties of laryngocarcinoma cells as well as the expression of bromodomain-containing protein 4 (BRD4), YAP1, and EMT markers were investigated. Moreover, the relationships between MALAT1 and miR-708-5p as well as between miR-708-5p and BRD4 were explored. Furthermore, whether MALAT1 regulated the malignant phenotypes of laryngocarcinoma cells via sponging miR-708-5p to target BRD4 was revealed by both in vitro and in vivo experiments. Results. MALAT1 suppression inhibited the malignant phenotypes of laryngocarcinoma cells, such as decreased proliferation, promoted apoptosis, suppressed migration, and inhibited the CSC properties. Suppression of MALAT1 increased miR-708-5p expression and decreased the expression of BRD4 and YAP1 and inhibited EMT. Moreover, there were target relationships between MALAT1 and miR-708-5p as well as between miR-708-5p and BRD4. miR-708-5p overexpression and MALAT1 suppression had synergistic inhibitory effects on the malignant phenotypes of laryngocarcinoma cells and the expression of BRD4, YAP1, and EMT. Furthermore, in vivo experiments confirmed that MALAT1/miR-708-5p regulated tumorigenicity by regulating BRD4 and YAP1-mediated EMT. Conclusions. Our results indicate that suppression of MALAT1 may inhibit laryngocarcinoma development by sponging miR-708-5p/BRD4 to regulate YAP1-mediated EMT. Targeting MALAT1/miR-708-5p/BRD4 axis may provide a promising therapeutic strategy for laryngocarcinoma.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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