MiR-1226, mediated by ASCL1, suppresses the progression of non-small cell lung cancer by targeting FGF2 - 02/05/22

Summary |
Objective |
This study aims to elucidate the characteristic and expression level of miR-1226 in non-small cell lung cancer (NSCLC) tissue samples and cell lines, and its potential influence on the malignant progression of NSCLC.
Methods |
The expression level of miR-1226 in tumor tissue and paracancerous tissue of NSCLC patients was detected by qRT-PCR. The influences on clinical features of NSCLC patients were analyzed. The proliferation and metastasis ability in H1299 and SPC-A1 cells were examined by CCK-8 and Transwell assay, respectively. Subsequently, the binding relationship between miR-1226 and FGF2 was verified by dual-luciferase reporter assay. The upstream regulatory factor ASCL1 was identified through database prediction, and the co-regulation on NSCLC cell lines was explored via rescue experiments.
Results |
miR-1226 was down-regulated in NSCLC tissue samples and cell lines, which suggested that miR-1226 was associated with tumor stage and lymph node metastasis. The transfection of miR-1226 mimic inhibited the proliferation and migration in H1299 and SPC-A1 cells. In addition, the overexpression of miR-1226 suppressed tumor growth in vivo. FGF2 was the downstream target binding miR-1226, which was up-regulated in NSCLC tissue samples. Moreover, ASCL1 was found to be a potential regulator of miR-1226. Finally, the tumor suppressive effect of miR-1226 was reversed by its downstream FGF2 and upstream factor ASCL1.
Conclusions |
miR-1226, which was regulated by ASCL1, inhibited tumor growth and migration by targeting FGF2, indicating that the ASCL1/miR-1226/FGF2 axis could be a potential therapeutic target for NSCLC.
Le texte complet de cet article est disponible en PDF.Keywords : miR-1226, ASCL1, FGF2, Non-small cell lung cancer
Plan
Vol 109 - N° 4
P. 424-435 - avril 2022 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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