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MCM3AP-AS1 promotes cisplatin resistance in gastric cancer cells via the miR-138/FOXC1 axis

The dysregulation of long non-coding RNAs (lncRNAs) serves a pivotal role in the pathogenesis and development of multiple types of human cancer, including gastric cancer (GC). MCM3AP-antisense 1 (MCM3AP-AS1) has been reported to function as a tumor promoter in various types of cancer. However, the b...

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Detalles Bibliográficos
Autores principales: Sun, Han, Wu, Ping, Zhang, Bao, Wu, Xia, Chen, Weixu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7836396/
https://www.ncbi.nlm.nih.gov/pubmed/33510812
http://dx.doi.org/10.3892/ol.2021.12472
Descripción
Sumario:The dysregulation of long non-coding RNAs (lncRNAs) serves a pivotal role in the pathogenesis and development of multiple types of human cancer, including gastric cancer (GC). MCM3AP-antisense 1 (MCM3AP-AS1) has been reported to function as a tumor promoter in various types of cancer. However, the biological function of MCM3AP-AS1 in the resistance of GC cells to cisplatin (CDDP) remains to be elucidated. The present study aimed to elucidate the mechanisms of MCM3AP-AS1 in the resistance of GC cells to CDDP. The expression levels of MCM3AP-AS1, miR-138 and FOXC1 were measured via reverse transcription-quantitative PCR. In addition, cell viability, migration and invasion were assessed via the Cell Counting Kit-8, wound healing and transwell assays, respectively. The interaction between genes was confirmed via the dual-luciferase reporter and pull-down assays. Western blot analysis was performed to detect FOXC1 protein expression. In the present study, it was demonstrated that MCM3AP-AS1 expression was upregulated in CDDP-resistant GC cells and that MCM3AP-AS1-knockdown suppressed CDDP resistance in GC cells. Moreover, the examination of the molecular mechanism indicated that MCM3AP-AS1 upregulated FOXC1 expression by sponging microRNA (miR)-138. Additionally, it was identified that the overexpression of FOXC1 abolished MCM3AP-AS1-knockdown- or miR-138 mimic-mediated inhibitory effects on CDDP resistance in GC cells. In conclusion, the present findings suggested that MCM3AP-AS1 enhanced CDDP resistance by sponging miR-138 to upregulate FOXC1 expression, indicating that MCM3AP-AS1 may be a novel promising biomarker for the diagnosis and treatment of patients with GC.