Background:

YL-109 is a novel anticancer agent which has ability to inhibit breast cancer cell growth and invasiveness in vitro and in vivo.IC50 value: 85.7 nM(MCF-7 cells proliferation) [1]Target: AhR signaling activcatorin vitro: YL-109 strongly inhibited cell proliferation of MCF-7 cells in a dose-dependent manner (IC50= 85.8 nM). Surprisingly, YL-109 had an anti-proliferative effect in a dose-dependent manner (IC50 = 4.02 μM) on MDA-MB-231 cells. YL-109 repressed the sphere-forming ability and the expression of stem cell markers in MDA-MB-231 mammosphere cultures. YL-109 increased the expression of carboxyl terminus of Hsp70-interacting protein (CHIP), which suppresses tumorigenic and metastatic potential of breast cancer cells by inhibiting the oncogenic pathway. YL-109 induced CHIP transcription because of the recruitment of the aryl hydrocarbon receptor (AhR) to upstream of CHIP gene in MDA-MB-231 cells. Consistently, the antitumor effects of YL-109 were depressed by CHIP or AhRknockdown in MDA-MB-231 cells [1].in vivo: Mice treated with vehicle showed significantly enlarged tumors, whereas mice treated with YL-109 showed attenuated tumor growth using MCF-7 cells. Interestingly, YL-109 also suppressed tumor growth in mice injected with MDA-MB-231 cells. Compared with the vehicle control, YL-109 significantly reduced lung metastasis [1].

参考文献:
[1]. Hiyoshi H, et al. 2-(4-Hydroxy-3-methoxyphenyl)-benzothiazole suppresses tumor progression and metastatic potential of breast cancer cells by inducing ubiquitin ligase CHIP. Sci Rep. 2014 Nov 18;4:7095.