Fig 1: Expressions of NR4A2, MAP3K8, CXCL8 and SLC7A11 in the Ishikawa cell line treated with either cisplatin or salinomycin and a control culture, obtained via the Western blot technique. C—control; H_12, H_24, H_48—periods of exposure to cisplatin or salinomycin; NR4A2—nuclear receptor subfamily 4 group A member 2; MAP3K8—mitogen-activated protein kinase kinase 8; CXCL8—C-X-C motif chemokine ligand 8; SLC7A11—solute carrier family 7 member 11.
Fig 2: Changes in the expression patterns of genes related to oxidative stress in an Ishikawa cell culture exposed to cisplatin (A) and salinomycin (B), in comparison to the control obtained via RTqPCR (p < 0.05). (+)—overexpression in comparison to the control; (-)—downregulated in comparison to the control; C—control; H_12, H_24, H_48—periods of exposure to cisplatin or salinomycin; NR4A2—nuclear receptor subfamily 4 group A member 2; MAP3K8—mitogen-activated protein kinase 8; ICAM1—intercellular adhesion molecule 1; IL21—interleukin 21; CXCL8—C-X-C motif chemokine ligand 8; CCL7—C-C motif chemokine ligand 7; SLC7A11—solute carrier family 7 member 11.
Fig 3: Variances in the concentration of the proteins NR4A2, MAP3K8, CXCL8 and SLC7A11 determined via ELISA assay in the Ishikawa cell line regardless of the time of incubation of endometrial cancer cells with either cisplatin (A) or salinomycin (B), in comparison with the control. C—control; H_12, H_24, H_48—periods of exposure to cisplatin or salinomycin; NR4A2—nuclear receptor subfamily 4 group A member 2; MAP3K8—mitogen-activated protein kinase kinase 8; CXCL8—C-X-C motif chemokine ligand 8; SLC7A11—solute carrier family 7 member 11; p—p-value.
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