The knockdown of miR-23b enhances radio-sensitivity of lung cancer A549 cell via targeting PTEN / 中国肿瘤生物治疗杂志
Chinese Journal of Cancer Biotherapy
; (6): 1113-1119, 2019.
Article
em Zh
| WPRIM
| ID: wpr-793234
Biblioteca responsável:
WPRO
ABSTRACT
@# Objective:
To investigate the effect of miR-23b/PTEN molecular axis on radio-sensitivity of lung cancerA549 cells and its mechanism.Methods:
Lung cancer cell lines NCI-H1650, NCI-H175, Calu-1, LT-P-A-2, MSTO-211H, A549 and human normal lung epithelial cell line BEAS-2B were selected. The expression level of miR-23b in lung cancer cell lines was detected by qPCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-23b and PTEN. Plasmids miR-23b mimics, miR-23b inhibitor and pcDNA3.1-PTEN were transfected intoA549 cells by lipofection; PTEN expression levels in cells was detected by WB. CCK-8, Transwell andAnnexin V-FITC/PI staining flow cytometry were used to detect the effect of miR-23b/PTEN axis on proliferation, invasion and apoptosis ofA549 cells treated with 60Co γ-ray.Results:
miR-23b was upregulated in lung cancer cell lines with the highest expression in A549 cells (P<0.05 or P<0.01). Knockdown of miR-23b reversed the inhibitory effect of 3 Gy 60Co γ-rays on proliferation and invasion of A549 cells, and induced apoptosis (P<0.05 or P<0.01). Dual-luciferase reporter gene assay results confirmed that miR23b could negatively regulate PTEN (P<0.05). Furthermore, knockdown of miR-23b up-regulated PTEN expression level, and furhter enhanced the inhibitory effect of 3 Gy 60Co γ-ray on the proliferation and invasion of A549 cells as well as induced apoptosis of A549 cells (P<0.05 or P<0.01).Conclusion:
Knockdown of miR-23b can enhance the radio-sensitivity of A549 cells, the mechanism of which is that 60Co γ-ray down-regulates the inhibitory effect of miR-23b on PTEN, thereby inhibiting the proliferation, invasion and inducing apoptosis ofA549 cells.
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Base de dados:
WPRIM
Tipo de estudo:
Diagnostic_studies
Idioma:
Zh
Ano de publicação:
2019
Tipo de documento:
Article