Fig. 5: GLI1 inhibitor GANT61 impaired the function of PGC7 on tumor lineage reversion both in vitro and in vivo. | Cell Death & Differentiation

Fig. 5: GLI1 inhibitor GANT61 impaired the function of PGC7 on tumor lineage reversion both in vitro and in vivo.

From: PGC7 promotes tumor oncogenic dedifferentiation through remodeling DNA methylation pattern for key developmental transcription factors

Fig. 5

a Expression of GLI1 and MYCN was detected by qRT-PCR with the treatment of 10 μM GANT61 for 48 h. b–d PGC7 overexpressing cells were pretreated with 10 μM GANT61 or DMSO solvent for 2 days, followed by sphere formation (b), ALDH activity characterization in MIHA cells (c), and in HCC organoids (d). e PGC7-overexpressed 97H and MIHA was treated with vehicle control, sorafenib (16 μM), GANT61 (10 μM), or the combined treatment of both drugs for 2 days, followed by apoptotic index detection. f PGC7-overexpressed HCC organoids were treated with vehicle control, sorafenib (8 μM), GANT61 (10 μM), or the combined treatment of both drugs for 5 days, and cell viability was detected by CellTiter-Glo assay. g Mice with established subcutaneous HCC tumors of similar size were randomly divided into four groups and were given vehicle control, 10 mg/kg sorafenib via oral gavage, 50 mg/kg GANT61 via intraperitoneal injection, or combined treatment. Sorafenib was given daily and GANT61 was administered every other day. The average tumor volume was expressed as the mean ± SD of 6 mice. h The tumors at the end of treatment (left panel) and a graph showing the weight of tumors at the end of treatment (right panel). Each dot represents a single tumor. Statistics: in a–h, Student’s t-test was used for statistical analysis, *P < 0.05, **P < 0.01, ***P < 0.001, data are shown as mean ± SD. Data represent at least three independent experiment.

Back to article page