期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 35, 期 3, 页码 926-932出版社
KARGER
DOI: 10.1159/000369749
关键词
beta-catenin; Wnt; Prostate cancer; Autophagy; Nitric oxide
Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit beta-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of beta-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of beta-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated beta-catenin signaling pathway for regulating autophagy in prostate cancer. Copyright (C) 2015 S. Karger AG, Basel
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据