id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-013544-x3eyimug	Hu, Yue-huai	sFRP1 protects H9c2 cardiac myoblasts from doxorubicin-induced apoptosis by inhibiting the Wnt/PCP-JNK pathway	2020-04-01		.txt	text/plain	4100	256	53	In this study, we investigated the relationship between sFRP1 and noncanonical Wnt/PCP-JNK (Wnt/planar cell polarity-c-Jun N-terminal kinase) pathway in Dox-induced cardiotoxicity in vitro and in vivo. We showed that treatment of H9c2 cardiac myoblasts with Dox (1 μM) time-dependently suppressed cell viability accompanied by significantly decreased sFRP1 protein level and increased Wnt/PCP-JNK signaling. Overexpression of sFRP1 protected H9c2 cells from Dox-induced apoptosis by inhibiting the Wnt/PCP-JNK pathway. The results described above indicated that the Wnt/PCP-JNK signaling pathway was involved in Dox-induced apoptosis of H9c2 cells. The results described above indicated that sFRP1 protected H9c2 cells from Dox-induced apoptosis by inhibiting the Wnt/PCP-JNK pathway. In addition, anisomycin treatment induced the activation of Wnt/PCP-JNK signaling and the apoptosis of the H9c2 cells, and these effects were suppressed by sFRP1. The results described above led to the conclusion that sFRP1 protected the H9c2 cells from Dox-induced apoptosis by inhibiting Wnt/PCP-JNK signaling.	./cache/cord-013544-x3eyimug.txt	./txt/cord-013544-x3eyimug.txt