Disruption of the unfolded protein response (UPR) by lead compound selectively suppresses cancer cell growth. Issue 2 (1st May 2015)

• Record Type: Journal Article
• Authors: Huang, Hejing; Liu, Huanan; Liu, Changmei; Fan, Lixia; Zhang, Xinwen; Gao, Anhui; Hu, Xiaobei; Zhang, Kunzhi; Cao, Xianchao; Jiang, Kailong; Zhou, Yubo; Hou, Jian; Nan, Fajun; Li, Jia
• Is Part Of: Cancer letters. Volume 360:Issue 2(2015)
• Page Start: 257
• Page End: 268
• Publication Date: 2015-05-01
• Subjects: Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2015.02.029
• Languages: English
• ISSNs: 0304-3835

Abstract

<abstract abstract-type="author-highlights" id="ab0010"> <title id="st0010">Highlights</title> <sec> <p id="sp0010"> <list id="ulist0010"> <list-item id="u0010"> <label></label> <p id="p0010">17#, a novel small-molecule compound, abrogates the UPR in cancer cells stressed by divergent ER stress stimuli.</p> </list-item> <list-item id="u0015"> <label></label> <p id="p0015">17# showed good selectivity for cell growth inhibition, cell cycle arrest and apoptosis in glucose-deprived status.</p> </list-item> <list-item id="u0020"> <label></label> <p id="p0020">17# alone suppress the growth of HeLa tumor xenografts, and has a synergistic anti-cancer effect with 2DG <italic>in vivo</italic>.</p> </list-item> <list-item id="u0025"> <label></label> <p id="p0025">17#-induced selective anti-cancer effects were highly dependent on UPR inhibition.</p> </list-item> <list-item id="u0030"> <label></label> <p id="p0030">Overexpressing GRP78 or XBP1s reversed the 17#-induced growth inhibition and cell cycle arrest.</p> </list-item> </list> </p> </sec> </abstract>