Por favor, use este identificador para citar o enlazar este ítem: https://doi.org/10.14670/HH-18-573

Título: MiR-101-3p targets KPNA2 to inhibit the progression of lung squamous cell carcinoma cell lines
Fecha de publicación: 2023
Editorial: Universidad de Murcia, Departamento de Biologia Celular e Histiologia
Cita bibliográfica: Histology and Histopathology Vol. 38, nº10 (2023)
ISSN: 0213-3911
1699-5848
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Lung squamous cell carcinoma
miR-1013p
KPNA2
Proliferation
Migration
Invasion
Apoptosis
Resumen: We herein discuss the impacts of miR-101-3p on the tumorigenesis-related cell behaviors in lung squamous cell carcinoma (LUSC) by repressing KPNA2. TCGA database was utilized to measure miR101-3p and KPNA2 levels in LUSC tissues and cells. The interaction of miR-101-3p and KPNA2-3’UTR was determined by dual luciferase assay. Western blot evaluated the protein level of KPNA2. MiR-101-3p was under-expressed in LUSC cells while KPNA2 was overexpressed. Western blot confirmed the impact of KPNA2 expression on cancer cell progression. The negative regulatory impact of miR-101-3p on KPNA2 was also verified. In vitro cell function assays revealed the suppressing effect of high miR-101-3p expression on cell invasion, migration and viability, as well as its promoting effect on apoptosis. Up-regulated miR-101-3p weakened the promoting effect of overexpressed KPNA2 on LUSC malignant progression. To conclude, miR-101-3p repressed viability, invasion, and migration, and facilitated cell apoptosis in LUSC by suppressing KPNA2.
Autor/es principal/es: Dong, Liangliang
Jiang, Hanliang
Qiu, Ting
Xu, Yiming
Chen, Enguo
Huang, Aihua
Ying, Kejing
URI: http://hdl.handle.net/10201/134423
DOI: https://doi.org/10.14670/HH-18-573
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 10
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Aparece en las colecciones:Vol.38,nº10 (2023)

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