LncRNA MALAT1 Regulated ATAD2 to Facilitate Retinoblastoma Progression Via MiR-655-3p

Overview

Journal Open Med (Wars)

Specialty General Medicine

Date 2021 Jul 5

PMID 34222668

Citations 9

Authors

Yuxin Zhao

Zhaoxia Wang

Meili Gao

Xuehong Wang

Hui Feng

Yuanyuan Cui

Xia Tian

Affiliations

Soon will be listed here.

Abstract

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB. MALAT1 was upregulated in RB tissues and cells, and it served as a competing endogenous RNA (ceRNA) and inhibited miRNA-655-3p (miR-655-3p) expression, which eventually regulated the expression of miR-655-3p downstream target ATPase Family AAA Domain Containing 2 (ATAD2). The level of ATAD2 significantly increased, while that of miR-655-3p remarkably decreased in RB tissues and cells. MALAT1 depletion inhibited cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT), but promoted apoptosis and blocked xenograft tumor growth . MALAT1 exerted its oncogenic functions in RB by regulating miR-655-3p/ATAD2 axis.

Citing Articles

Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases.

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The clinical diagnostic value of plasma miR-592 and miR-217-3p levels in retinoblastoma.

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