N6‐methyladenosine‐mediated LINC01087 promotes lung adenocarcinoma progression by regulating miR‐514a‐3p to upregulate centrosome protein 55

Abstract

AbstractLong noncoding RNAs are key players in the development of lung adenocarcinoma (LUAD). The present study elucidated the role of LINC01087 in LUAD development. Cell vitality and apoptosis were assessed by the CCK‐8 assay and flow cytometry, respectively. The transwell assay was adopted to evaluate cell migration and invasion. Levels of m6A modification of LINC01087 were determined using the methylated RNA binding protein immunoprecipitation assay. The interactions among LINC01087, miR‐514a‐3p, and centrosome protein 55 (CEP55) were evaluated using dual‐luciferase reporter, RNA immunoprecipitation, and RNA–RNA pull‐down assays. LINC01087 was highly expressed in LUAD, and its downregulation restrained cancer cell proliferation, migration, invasion, and epithelial–mesenchymal transition in vitro as well as tumor growth in a xenograft tumor model. Overexpression of miR‐514a‐3p inhibited malignant phenotypes in LUAD cells by inactivating RhoA/ROCK1 signaling via the suppression of CEP55 expression. Mechanistically, RBM15 increased the expression and mRNA stability of LINC01087 by mediating its m6A modification and LINC01087 induced CEP55 expression by sponging miR‐514a‐3p. RBM15‐induced LINC01087 upregulation accelerated LUAD progression by regulating the miR‐514a‐3p/CEP55/RhoA/ROCK1 axis, illustrating the potential of LINC01087 as a novel target for LUAD therapy.