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Long noncoding RNA MALAT1 knockdown inhibits progression of anaplastic thyroid carcinoma by regulating miR-200a-3p/FOXA1

Authors
  • Gou, Lisha1
  • Zou, Huawei2
  • Li, Beibei1
  • 1 Department of Endocrine, Zhoukou Central Hospital, China , (China)
  • 2 Department of Thyroid Surgery, Zhoukou Central Hospital, China , (China)
Type
Published Article
Journal
Cancer Biology & Therapy
Publisher
Landes Bioscience
Publication Date
Sep 10, 2019
Volume
20
Issue
11
Pages
1355–1365
Identifiers
DOI: 10.1080/15384047.2019.1617567
PMID: 31500506
PMCID: PMC6804806
Source
PubMed Central
Keywords
License
Unknown

Abstract

Long noncoding RNAs (lncRNAs) have been reported to play essential roles in progression of thyroid carcinoma. However, the roles of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in anaplastic thyroid carcinoma (ATC) process and its mechanism remain not been fully established. In this study, we focused on the effect of MALAT1 on cell proliferation, apoptosis, migration, invasion, and autophagy formation in ATC and explored the interaction between miR-200a-3p and MALAT1 or FOXA1. Moreover, murine xenograft model was established to investigate the roles and mechanism of MALAT1 in ATC progression in vivo . Results showed that MALAT1 expression was enhanced and miR-200a-3p was reduced in ATC tissues and cells. Knockdown of MALAT1 or overexpression of miR-200a-3p inhibited cell proliferation, migration and invasion but increased apoptosis and autophagy formation in ATC cells. Moreover, miR-200a-3p was directly bound to MALAT1 and its inhibition reversed the inhibitory effect of MALAT1 knockdown on progression of ATC. In addition, FOXA1 was indicated as a target of miR-200a-3p and its restoration attenuated the anti-cancer role of miR-200a-3p in ATC cells. Furthermore, MALAT1 functioned as a competing endogenous RNA (ceRNA) via sponging miR-200a-3p to derepress FOXA1 expression. Besides, interference of MALAT1 decreased tumor growth by upregulating miR-200a-3p and downregulating FOXA1. Collectively, MALAT1 knockdown suppressed ATC progression by regulating miR-200a-3p/FOXA1, providing a novel avenue for treatment of ATC.

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