Korean J Physiol Pharmacol 2023; 27(3): 197-208
Published online May 1, 2023 https://doi.org/10.4196/kjpp.2023.27.3.197
Copyright © Korean J Physiol Pharmacol.
Lin Xu#, Daiting Liu#, and Xun Wang*
Digestion Medicine Department, Wuchang Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430063, China
Correspondence to:Xun Wang
#These authors contributed equally to this work.
Author contributions: L.X. and D.L. performed the experiments and the analysis of the data. X.W. designed and devised the study. L.X. obtained the data. D.L. and X.W. processed and interpreted the data. The manuscript has been read and approved by all authors.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Dysregulation of certain long non-coding RNAs may facilitate tumor initiation and progression. However, numerous carcinogenesis-related long non-coding RNAs have not been characterized. The goal of this study was to elucidate the role of LINC00562 in gastric cancer (GC). The expression of LINC00562 was analyzed using real-time quantitative PCR and Western blotting. The proliferative capacity of GC cells was determined using Cell Counting Kit-8 and colony-formation assays. The migration of GC cells were evaluated using wound-healing assays. The apoptosis of GC cells was assessed by measuring the expression levels of apoptosis-related proteins (Bax and Bcl-2). Xenograft models in nude mice were constructed for in vivo functional analysis of LINC00562. The binding relationship between miR-4636 and LINC00562 or adaptor protein complex 1 sigma 3 (AP1S3), obtained from public databases, was confirmed using dual-luciferase and RNA-binding protein immunoprecipitation experiments. LINC00562 was expressed in GC cells at high levels. Knockdown of LINC00562 repressed GC cell growth and migration, promoted apoptosis in vitro, and inhibited tumor growth in nude mouse models. LINC00562 directly targeted miR-4636, and miR-4636 depletion restored the GC cell behavior inhibited by LINC00562 absence. AP1S3, an oncogene, binds to miR-4636. MiR-4636 downregulation increased AP1S3 level, restoring GC cell malignant behaviors inhibited by AP1S3 downregulation. Thus, LINC00562 exerts carcinogenic effects on GC development by targeting miR-4636-mediated AP1S3 signaling.
Keywords: Competitive endogenous RNA, Long noncoding RNA, MicroRNA, Stomach neoplasms
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