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
Authors: Guigang Yan
Shujun Liu
Lianzhi Yu
Junfu Zhang
Journal: Oncology research (2018)
Discipline: CLINICAL MEDICINE
Keywords: lncRNA; MALAT1; retinoblastoma; miR-124; Y79 cell line
Affiliations: 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.

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 &lt; 0.01). Moreover, MALAT1 silence inhibited cell viability, migration, and invasion and promoted apoptosis in Y79 cells (p &lt; 0.05, p &lt; 0.01, or p &lt; 0.001). miR-124 was upregulated by MALAT1 silence and hence was identified as a target of MALAT1 (p &lt; 0.05 or p &lt; 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 &lt; 0.05, p &lt; 0.01, or p &lt; 0.001). In addition, Slug was a target of miR-124 and regulated cell viability, migration, invasion, and apoptosis in Y79 cells (p &lt; 0.05, p &lt; 0.01, or p &lt; 0.001). Further, Slug silence abolished miR-124 suppression-induced inactivation of the ERK/MAPK and Wnt/Œ≤-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/Œ≤-catenin signaling pathways in RB, which might provide a new approach for the treatment of RB. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader. This paper is one of a set of six papers that all share the same authors, were all published in 2014-2015, and that all share very similar plots. No matter what animal species (mouse, chicken, or ferret) or number of animals per group (6-25), the body weight loss in unprotected animals was all very similar (around 25% loss at day 6), while the protected animals all show a dip in body weight around 6 days, followed by an increase. In addition, the error bars (standard deviations in all papers) are unexpectedly small for these types of measurements. Could the authors please provide some explanation for these similarities? The 6 papers are the following: * Han Lei et al. Virology 476 (2015) 189u2013195, DOI: 10.1016 j.virol.2014.12.017, https: pubpeer.com publications E932C6D86F69113141665259EB4C79 * Han Lei et al. Arch Virol (2015) 160:3011u20133019, DOI: 10.1007 s00705-015-2587-8, https: pubpeer.com publications 4E88CDED2683B085DE9D52B7AD7700 * Han Lei et al. BMC Veterinary Research (2015) 11:85, DOI: 10.1186 s12917-015-0399-4, https: pubpeer.com publications B407285D6C4C238DC25A4FA0F28991 * Han Lei et al. Virus Research 196 (2015) 56u201359, DOI: 10.1016 j.virusres.2014.11.009, https: pubpeer.com publications 889BA6B1AE96E94614521AA9583E87 * Han Lei et al. Microb Cell Fact (2015) 14:111, DOI: 10.1186 s12934-015-0287-4, https: pubpeer.com publications A13874959B0962999C5A01039B8D02 * Han Lei et al. Journal of Medical Virology (2014), DOI: 10.1002 jmv.23983, https: pubpeer.com publications BFBF1A36BD6B9C54611A9727DA0206 And here are the graphs:      ,