LncRNA MALAT-1 competitively regulates miR-124 to promote EMT and development of non-small-cell lung cancer
Authors: Lin Cai
Fei He
Dong Liang
Yueyue Weng
Jiasheng Wu
Journal: Anti-cancer drugs (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: LncRNA MALAT-1; miR-124; epithelial-mesenchymal transition; non-small-cell lung cancer; NSCLC
Affiliations: The School of Public Health, Fujian Medical University., School of Design, Fujian University of Technology, Fuzhou, People's Republic of China.

Abstract:  This study was carried out to explore the mechanism of LncRNA MALAT-1 as a competing endogenous RNA to regulate miR-124 in epithelial-mesenchymal transition and development of non-small-cell lung cancer (NSCLC). NSCLC and adjacent tissues were collected for RT-qPCR. The correlation of MALAT-1 and miR-124 was analyzed by Pearson. MALAT-1 expression was measured in NSCLC A549, NCI-H460, NCI-H529, SK-MES-1 cells, and 16HBE cells. A549 cells were selected for cell transfection experiments after the creation of six groups. Luciferase reporter assay and RNA immunoprecipitation were used to verify the relationship between MALAT-1 and miR-124. Expressions of E-cadherin and vimentin were determined by western blot. Cell variability, apoptosis, invasion, and migration were measured by MTT, FCM, transwell assay, and scratch test. LncRNA MALAT-1 expression was higher in NSCLC tissues than that in adjacent tissues, but a lower expression of miR-124 was detected in the former tissues than in the latter tissues. Compared with 16HBE cells, MALAT-1 was highly expressed in NSCLC tissues. Compared with the blank group, E-cadherin and cell apoptosis were increased, but vimentin, cell variability, cell invasion, and migration ability in the si-MALAT-1 and miR-124 mimics groups were reduced. Compared with the blank group, decreased E-cadherin and cell apoptosis and increased vimentin, cell variability, cell invasion, and migration ability were detected in the oe-MALAT-1 group. The oe-MALAT-1+miR-124 mimics group had increased E-cadherin and cell apoptosis, but decreased vimentin, cell variability, cell invasion, and migration ability in comparison with the oe-MALAT-1 group. By competitively regulating miR-124, MALAT-1 can promote epithelial-mesenchymal transition, thus accelerating the development of NSCLC. 

Retracted: No

PubPeer comments:
 Fig 2E. ![file] Fig 3E. ![file] Fig 6E. ![file] Each panel contains a halo of regularly-spaced dots, surrounding a central clump with a curious texture, almost woven in appearance (see e.g. [Wang, Zhao Wang 2020] for similar results). Perhaps these are instrumentation artefacts of some kind. Is it possible for the authors to upload the raw data files to a data repository somewhere? , 
 It appears that many of the microscopic photographs in this paper overlap with others, sometimes with some differences in internal features. I have marked up those images in Figure 2F as an example, but there are more. Boxes indicate apparent areas of overlap, circles indicate apparent areas of difference. *** ![file] , 
 Retracted [5 October 2021] . -------------------------- The Editor and Publisher of Cancer Management and Research wish to retract the published article. Concerns were raised over the flow cytometry data presented in the article and over alleged image duplication in Figures 2F, 3F and 6C, specifically: - Figure 2F panel KNS-81 si-NC appears to show duplication with regions from panel KALS-1 si-NC. - Figure 2F panel KNS-81 SNHG1 appears to show duplication with regions from panel KALS-1 SNHG1. - Figure 3C panel KALS-1 miR-NC appears to show duplication with regions from Figure 6C panel KNS-81 si-NC. The authors responded to our queries but were unable to provide a satisfactory reason for the alleged duplication and were unable to provide any original data for their study. The Editor advised for the paper to be retracted. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. ,