LncRNA linc00460 sponges miR-1224-5p to promote esophageal cancer metastatic potential and epithelial-mesenchymal transition.


Journal

Pathology, research and practice
ISSN: 1618-0631
Titre abrégé: Pathol Res Pract
Pays: Germany
ID NLM: 7806109

Informations de publication

Date de publication:
Jul 2020
Historique:
received: 19 02 2020
revised: 28 04 2020
accepted: 15 05 2020
entrez: 15 6 2020
pubmed: 15 6 2020
medline: 2 4 2021
Statut: ppublish

Résumé

Increasing studies highlight the crucial role of long non-coding RNAs (lncRNAs) in carcinogenesis of various human cancer types, including esophageal cancer (ESCA). Long intergenic non-coding RNA 00460 (Linc00460), a novel oncogenic lncRNA, has been reported to accelerate ESCA cell growth. This study aimed to investigate the role and possible regulatory mechanism of linc00460 in ESCA metastasis. Bioinformatics analysis and quantitative real time polymerase chain reaction (qRT-PCR) were used to detect linc00460 expression in ESCA. Wound healing assay, Transwell assay and Western blot were utilized to examine migration, invasion and epithelial-mesenchymal transition (EMT) of ESCA cells. The direct binding effect between linc00460 and microRNA-1224-5p (miR-1224-5p) was evaluated by the dual luciferase reporter assay. In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines. Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells. In addition, miR-1224-5p, a potential tumor suppressor, was negatively correlated with linc00460 in ESCA. Linc00460 and miR-1224-5p could bind directly in ESCA cells. Inhibition of miR-1224-5p partially abrogated the effects of linc00460 decrease on metastatic potential and EMT of ESCA cells. Taken together, linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. Our findings suggest that linc00460/miR-1224-5p is a possible clinical target for ESCA.

Sections du résumé

BACKGROUND BACKGROUND
Increasing studies highlight the crucial role of long non-coding RNAs (lncRNAs) in carcinogenesis of various human cancer types, including esophageal cancer (ESCA). Long intergenic non-coding RNA 00460 (Linc00460), a novel oncogenic lncRNA, has been reported to accelerate ESCA cell growth. This study aimed to investigate the role and possible regulatory mechanism of linc00460 in ESCA metastasis.
METHODS METHODS
Bioinformatics analysis and quantitative real time polymerase chain reaction (qRT-PCR) were used to detect linc00460 expression in ESCA. Wound healing assay, Transwell assay and Western blot were utilized to examine migration, invasion and epithelial-mesenchymal transition (EMT) of ESCA cells. The direct binding effect between linc00460 and microRNA-1224-5p (miR-1224-5p) was evaluated by the dual luciferase reporter assay.
RESULTS RESULTS
In this study, we discovered that lncRNA linc00460 was obviously over-expressed in ESCA, both in tissues and cell lines. Down-regulation of linc00460 significantly suppressed the metastatic potential (including cell migration and invasion) and EMT of ESCA cells. In addition, miR-1224-5p, a potential tumor suppressor, was negatively correlated with linc00460 in ESCA. Linc00460 and miR-1224-5p could bind directly in ESCA cells. Inhibition of miR-1224-5p partially abrogated the effects of linc00460 decrease on metastatic potential and EMT of ESCA cells.
CONCLUSIONS CONCLUSIONS
Taken together, linc00460 may function as a molecular sponge to adsorb miR-1224-5p, thereby promoting ESCA metastasis and EMT. Our findings suggest that linc00460/miR-1224-5p is a possible clinical target for ESCA.

Identifiants

pubmed: 32534700
pii: S0344-0338(20)30491-X
doi: 10.1016/j.prp.2020.153026
pii:
doi:

Substances chimiques

MIRN1224 microRNA, human 0
MicroRNAs 0
RNA, Long Noncoding 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

153026

Informations de copyright

Copyright © 2020 Elsevier GmbH. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All of the authors declare that they have no conflict of interest.

Auteurs

Yuanbo Cui (Y)

School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China. Electronic address: cuiyuanbo18@126.com.

Chunyan Zhang (C)

Department of Clinical Laboratory, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.

Hongkai Lian (H)

Department of Orthopedics, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.

Linsen Xie (L)

Department of Clinical Laboratory, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.

Jinhui Xue (J)

Department of Pathology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, 450007, China.

Ningwei Yin (N)

Department of General Surgery, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.

Fangxia Guan (F)

School of Life Sciences, Zhengzhou University, Zhengzhou 450001, China. Electronic address: fxguan@126.com.

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Classifications MeSH