Fig. 3: Inflammation response facilitates the development and stemness of PGCCs. | Oncogenesis

Fig. 3: Inflammation response facilitates the development and stemness of PGCCs.

From: IL-6 promotes drug resistance through formation of polyploid giant cancer cells and stromal fibroblast reprogramming

Fig. 3

A, B PGCC formation (at recovery day 3) was inhibited by IL-6R antibody and apigenin in a dose-dependent manner, which was confirmed by population percentage (A, via flow cytometry; PGCCs, DNA content>4 C as grouped by grey arrows.) and morphological observation (B, DNA was labeled with H2B-GFP). Bars, 50 µm. C, D Spheroid formation (>=200 µm in diameter) capability of PGCCs was inhibited by apigenin (Api) and IL-6R antibody at day 7. In Hey cells, the number of spheroids developed after treatment with paclitaxel (PTX), PTX + anti-IL-6R, and PTX + Api were 46.7 ± 7.7, 11.7 ± 2.1, and 10.5 ± 1.1, respectively. In SKOV3 cells, the number of spheroids in each subgroup was 11.0 ± 2.0, 2.3 ± 0.5, and 1.7 ± 0.6, respectively. Bars, 200 µm. E Expression of embryonic markers including OCT4, NANOG, and SOX2 in PGCCs (recovery day 7) was downregulated by IL-6 knockdown (IL-6 shRNA), blocking with IL-6R antibody, apigenin, and IL-6R antibody + Api. Bars, 50 µm.

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