Open Access

ARTICLE

Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis by Targeting miR-124 in Retinoblastoma

Shujun Liu^*1, Guigang Yan^*1, Junfu Zhang^†, Lianzhi Yu^‡

* Department of Ophthalmology, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong, P.R. China
† Department of Ophthalmology, Weifang People’s Hospital, Weifang, Shandong, P.R. China
‡ Department of Physical Examination, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai, Shandong, P.R. China
1 These authors are co-first authors.

Oncology Research 2018, 26(4), 581-591. https://doi.org/10.3727/096504017X14953948675403

Retracted 25 July 2024

Abstract

Evidence suggests that the long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is upregulated in cancer tissues, and its elevated expression is associated with hyperproliferation. However, the underlying mechanisms regarding the role of MALAT1 in retinoblastoma (RB) remain unclear. This study aimed to explore the functional role of MALAT1 in RB by targeting miR-124. The results showed that the expression of MALAT1 was significantly higher in the Y79 cell line than in the ARPE-19 cell line (p<0.01). Moreover, MALAT1 silence inhibited cell viability, migration, and invasion and promoted apoptosis in Y79 cells (p< 0.05, p<0.01, or p<0.001). miR-124 was upregulated by MALAT1 silence and hence was identified as a target of MALAT1 (p<0.05 or p<0.001). In addition, miR-124 suppression inhibited cell apoptosis and remarkably abolished the inhibitory effects of MALAT1 silence on cell viability, migration, and invasion (p< 0.05, p<0.01, or p<0.001). In addition, Slug was a target of miR-124 and regulated cell viability, migration, invasion, and apoptosis in Y79 cells (p< 0.05, p<0.01, or p<0.001). Further, Slug silence abolished miR-124 suppression-induced inactivation of the ERK/MAPK and Wnt/β-catenin pathways. Taken together, our data highlight the pivotal role of MALAT1 in RB. Moreover, the present study elucidated the MALAT1–miR-124–ERK/MAPK and Wnt/β-catenin signaling pathways in RB, which might provide a new approach for the treatment of RB.

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