Fig. 5

PMCA inhibitor could suppress tumor growth in a xenograft model of metabolic and drug-resistant cancer. A (S-231) and B (S-MCF-7) Changes in relative tumor volumes (left), dissected tumor weights (middle), and body weight (right) of selected cells (each group, n = 10). Tumors were established in athymic nude mice and treated with 2DG (2-deoxy-d-glucose), caloxin, and candidate 13, each agent administered alone or in combination with 2DG. Data are presented as means ± SEM. C Characteristics of all examined patient-derived subtypes of cancer cell lines. D Whole gene variance in patient-derived drug-resistant cancer cells, YUMC-C1, YUMC-C2, and YUMC-P1, were compared with patient-derived drug-sensitive cancer cells, YUMC-M1. E Bar plot showing 15 significantly enriched upregulated pathways in patient-derived drug-resistant cancer cells (top: YUMC-C1, middle: YUMC-C2, bottom: YUMC-P1). F Heatmap of RNA-Seq expression values of target genes in patient-derived drug-resistant cancer cells. G Protein–protein interaction network functional enrichment analysis indicated PGC1α, HNF4α, and NFκB interaction from the STRING database. H (YUMC-C1), I (YUMC-C2), and J (YUMC-P1) Changes in relative tumor volumes (left), dissected tumor weights (middle), and body weight (right) of patient-derived drug-resistant cancer cells (each group, n = 10). Tumors were established in NOG mice and treated with oxaliplatin, sorafenib, caloxin, and candidate 13, each agent treated alone or in combination with oxaliplatin or sorafenib, and caloxin or candidate 13. Data are presented as means ± SEM. *P < 0.05 vs. control, **P < 0.01 vs. control, #P < 0.05 vs. oxaliplatin or sorafenib, ##P < 0.01 vs. oxaliplatin or sorafenib