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

Zhang, Xin; Wang, Dong-Jie; Jia, Li; Zhang, Wei

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

Zhang, Xin; Wang, Dong-Jie; Jia, Li; Zhang, Wei.

Afiliación

Zhang X; Department of Respiratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Wang DJ; Department of Respiratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jia L; Department of Respiratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhang W; Department of Respiratory, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Kaohsiung J Med Sci ; 40(9): 801-818, 2024 Sep.

Article en En | MEDLINE | ID: mdl-39023191

ABSTRACT

ABSTRACT

Long 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.

Asunto(s)

Adenocarcinoma del Pulmón; Adenosina; Proteínas de Ciclo Celular; Movimiento Celular; Proliferación Celular; Regulación Neoplásica de la Expresión Génica; Neoplasias Pulmonares; MicroARNs; ARN Largo no Codificante; Humanos; MicroARNs/genética; MicroARNs/metabolismo; ARN Largo no Codificante/genética; ARN Largo no Codificante/metabolismo; Neoplasias Pulmonares/genética; Neoplasias Pulmonares/patología; Neoplasias Pulmonares/metabolismo; Adenocarcinoma del Pulmón/genética; Adenocarcinoma del Pulmón/patología; Adenocarcinoma del Pulmón/metabolismo; Proteínas de Ciclo Celular/genética; Proteínas de Ciclo Celular/metabolismo; Animales; Adenosina/análogos & derivados; Adenosina/metabolismo; Movimiento Celular/genética; Línea Celular Tumoral; Ratones; Proteína de Unión al GTP rhoA/metabolismo; Proteína de Unión al GTP rhoA/genética; Quinasas Asociadas a rho/metabolismo; Quinasas Asociadas a rho/genética; Proteínas de Unión al ARN/metabolismo; Proteínas de Unión al ARN/genética; Transición Epitelial-Mesenquimal/genética; Progresión de la Enfermedad; Regulación hacia Arriba; Proteínas Nucleares/metabolismo; Proteínas Nucleares/genética; Apoptosis/genética; Ratones Desnudos; Transducción de Señal; Masculino

Palabras clave

LINC01087; RNA binding motif protein 15; centrosome protein 55; lung adenocarcinoma; miR514a3p

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación Neoplásica de la Expresión Génica / Adenosina / Movimiento Celular / Proteínas de Ciclo Celular / MicroARNs / Proliferación Celular / ARN Largo no Codificante / Adenocarcinoma del Pulmón / Neoplasias Pulmonares Idioma: En Revista: Kaohsiung J Med Sci Asunto de la revista: MEDICINA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación:

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