Fig. 5

Olaparib- and Oligo-Fucoidan-treated TNBC cells promote M1 macrophage plasticity and inhibit the oncogenic and glycolytic pathways. A The F4/80(+) M0 macrophage population was examined by flow cytometry (n = 6) after THP-1 monocytes were treated with PMA (100 ng/ml) for 72 h. B, C MDA-MB-231 cells were pretreated with olaparib (50 μM) and/or Oligo-Fucoidan (400 μg/ml) for 48 h and cultured in serum-free medium for 48 h, after which the conditioned medium (CM) was collected and incubated with M0 macrophages for 48 h and 72 h to examine the polarity of CD80(+) M1 (B) and CD163(+) M2 macrophages (C) by flow cytometry (n = 6). D IL-6, EGFR/p-EGFR (Tyr1068), AMPK/p-AMPK (Thr172), PD-L1 and glucose metabolism factors (Glut1, PFKL, RPIA, PKM2/p-PKM2 (Tyr105), HK2, MCT4) were examined in MAD-MB-231 and 4T1 cells after olaparib (50 μM) and/or Oligo-Fucoidan (400 μg/ml) treatment for 24 h. E, F Glycolytic pathways, such as glucose uptake (E) and lactate production (F), were analyzed in TNBC cell lines after the indicated treatments for 24 h (n = 4). The data represent the mean ± SD. Student’s t test (A) and one-way ANOVA with Duncan’s test (B, C, E, F) were used to calculate statistical significance