Fig. 9

Tumoral c-Jun promotes chemotherapy resistance of GEM through dual pathways including stemness and iron metabolism in PDAC. A-B Each PDX1# primary cell line was treated with GEM (0.8 μM) for 72 h, and then cellular apoptosis in indicated cell lines were analyzed by flow cytometry. PBS was used as vehicle control. The representative dot plots were shown (A) and statistical analysis was shown (B). C The IC50 value of gemcitabine in indicated cell lines were determined by CCK-8. D-E Indicated PDX1# primary cell line was subcutaneously transplanted into BALB/C-nude mice and then GEM was administrated. Representative images of tumors were shown (D) and tumor weights were monitored (E). F Indicated PDO1# line was treated with GEM (0.8 μM) for 72 h, and then cellular viability in indicated PDO line was analyzed by CellTiterGlo-3D assay. PBS was used as vehicle control. Statistical analysis of organoid viability was shown. All experiments were repeated three times independently. Paired Student’s t-test were used for in vitro experiments. Un-paired Student’s t-test were used for in vivo experiments