Fig. 4

Enhancement of target therapy-induced proliferation inhibition by GPR119 agonists. a Cell proliferation was monitored after treatments with vehicle or 4-OHT (0.3-10 μM). b and c Cell proliferation was monitored after treatments with 0.3 μM 4-OHT and GPR119 agonists (1-10 μM). Data represent the mean ± S.D. (n=6). d LC3B I/II were measured by western blottings in breast cancer cells incubated with 0.3 μM 4-OHT in the presence or absence of 10 μM MBX for 24 h. e Expression levels of GPR119 mRNA in three human hepatocellular carcinoma cell lines were verified by real-time qPCR. f HepG2 cells were incubated with 10 μM sorafenib or MBX (1-10 μM) for 48 h, and cell proliferation was monitored by MTT assays. Data represent the mean ± S.D. (n=6). g Autophagy induction by sorafenib in HepG2 cells. The cells were incubated with vehicle or sorafenib (1-30 μM) for 18 h. h ATG7 expression was detected by western blotting after siATG7 transfection (left) and cell proliferation was monitored by Incucyte® ZOOM basic analyzer in HepG2 cells (right). Data represent the mean ± S.D. (n=6). i LC3B I/II were measured by western blottings in HepG2 cells incubated with 10 μM sorafemib in the presence or absence of MBX (3 and 10 μM) or 3 μM chloroquine for 18 h. j Cells were incubated with sorafenib in the presence or absence of MBX (1-10 μM) for 24 h. k In vivo effect of MBX-2982 on tumor growth of HepG2-X xenograft. Sorafenib (10 mg/kg), MBX-2982 (10 mg/kg) or Sorafenib with MBX-2982 were orally administered (5 times a week) and tumor growth was monitored for 18 days. Data represent the mean ± S.E. (n=6). * p < 0.05, *** p < 0.005, significant difference between the two indicated groups