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Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis

LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by in situ hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, a...

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Detalles Bibliográficos
Autores principales: Huang, Xing, Wang, Zihe, Hou, Shengzhong, Yue, Chao, Li, ZhenLu, Hu, Weiming, Lu, Huimin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973590/
https://www.ncbi.nlm.nih.gov/pubmed/35142595
http://dx.doi.org/10.1080/21655979.2021.2016326
Descripción
Sumario:LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by in situ hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An in vivo animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.