下调和上调
细胞生长
细胞生物学
基因敲除
细胞迁移
生物
基因沉默
癌症研究
肿瘤坏死因子α
细胞
内分泌学
细胞培养
生物化学
遗传学
基因
标识
DOI:10.1016/j.intimp.2020.106366
摘要
The thyroid receptor interactor protein 6 (TRIP6) has emerged as a key regulator for the proliferation and migration of various cells. However, whether TRIP6 is involved in regulating the proliferation and migration of airway smooth muscle (ASM) cells in the progression of pediatric asthma remains undetermined. The present study investigated the function of TRIP6 in regulating the proliferation and migration of fetal ASM cells induced by tumor necrosis factor (TNF)-α in vitro. The results revealed that TRIP6 expression was significantly upregulated in TNF-α-stimulated ASM cells. Loss-of-function experiments demonstrated that the knockdown of TRIP6 markedly suppressed TNF-α-proliferation and migration of ASM cells. By contrast, overexpression of TRIP6 had the opposite effect. In-depth research uncovered that TNF-α stimulation promoted the activation of yes-associated protein (YAP), which could be significantly reversed by TRIP6 silencing. Moreover, inactivation of YAP significantly reversed the promotion effect of TRIP6 overexpression on TNF-α-induced ASM cell proliferation and migration. Overall, these results reveal that upregulation of TRIP6 contributes to the proliferation and migration of fetal ASM cells by enhancing YAP activation, highlighting the importance of the TRIP6/YAP axis in the airway remodeling of pediatric asthma.
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