LINC02381 Silencing Repressed EML4-ALK+ Lung Cancer Cell Proliferation, Migration and Invasion via miR-133b/ALK Axis

Abstract

Background: Long non-coding RNAs (lncRNAs) have been intensively expounded to be implicated in various cancers, including lung cancer (LC), where LINC02381 is highly expressed in lung adenocarcinoma, but its function on LC is poorly defined. Additionally, echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) functions as a prominent pathogenic factor in NSCLC, one major subtype of LC. This paper is designed to investigate whether and how LINC02381 affects EML4-ALK⁺ LC progression. Methods: EML4-ALK⁺cells were transfected with small interfering RNA (siRNA) for LINC02381 (LIN-siRNA). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was made to test ALK, miR-133b and LINC02381 expression levels. The targeting relationship between LINC02381 and miR-133b or miR-133b and ALK was predicted and verified through bioinformatics analysis and dual-luciferase reporter assay. The proliferative, migratory and invasive abilities of cells were evaluated by 5-ethynyl-2’-deoxyuridine (EdU), colony formation, wound healing and Transwell assays. Results: LINC02381 expression levels were upregulated in EML4-ALK⁺ LC cells. LINC02381 targeted miR-133b and miR-133b targeted ALK. LINC02381 silencing promoted miR-133b expression to down-regulate ALK levels in EML4-ALK⁺ LC cells. LINC02381 silencing repressed EML4-ALK⁺ LC cell proliferation, migration and invasion. Conclusions: LINC02381 silencing inhibits EML4-ALK⁺ LC cell proliferation, migration and invasion via the miR-133b/ALK axis.