Fig 2: Correlations between COX−2 and its transcription factors (NF−κB, Sp1, and c−Jun) in PDAC tissues. (A) Positive correlation between COX−2 and cytoplasmic NF−κB expression. (B) Positive correlation between COX−2 and nuclear NF−κB expression. (C) Positive correlation between COX−2 and Sp1 expression. (D) Positive correlation between COX−2 and c−Jun expression. (E) Positive correlation between cytoplasmic and nuclear NF−κB expression. COX−2, cyclooxygenase−2; NF−κB, nuclear factor kappa−B; and Sp1, specificity protein 1. * p < 0.01.

Fig 3: The difference in NF−κB, COX−2, Sp1, and c−Jun expressions between PDAC tissue and adjacent normal tissue. COX−2, cyclooxygenase−2; NF−κB, nuclear factor kappa−B; and Sp1, specificity protein 1. * p < 0.05.

Fig 4: Positive and negative immunohistochemistry staining patterns of each protein. The most dominant stain of COX−2 in our specimens was in the cytoplasm. (A) An example of positive COX−2 cytoplasmic staining, and (B) an example of negative COX−2 cytoplasmic staining. The most dominant stain of NF−κB RelA/p65 in our specimens was also in the cytoplasm, although nuclear staining could also be seen. (C) An example of positive NF−κB RelA/p65 cytoplasmic staining, and (D) an example of negative NF−κB RelA/p65 cytoplasmic staining. (E) An example of positive NF−κB RelA/p65 nuclear staining, and (F) an example of negative NF−κB RelA/p65 nuclear staining. The most dominant stains of Sp1 and c−Jun in our specimens were in the nucleus. (G) An example of positive Sp1 nuclear staining, and (H) an example of negative Sp1 nuclear staining. (I) An example of positive c−Jun nuclear staining, and (J) an example of negative c−Jun nuclear staining. Images were taken at 400× magnification. COX−2, Cyclooxygenase−2; NF−κB, Nuclear Factor Kappa−B; Sp1, Specificity Protein 1.

Fig 5: IL-27 induces decidual COX-2+ macrophage differentiation in vitro.(A and B) Expression of IL-27RA in DSCs (n = 9), trophoblast cells (Tros; n = 9), DLCs (n = 9), and decidual macrophages (dMφs) (n = 9) was analyzed by FCM. Statistical graph of (A) was shown in (B). (C and D) Expression of p-STAT3 and STAT3 in dMφs (n = 9) after coculture with ESCs pretreated with FBP (0.5 mM for 24 hours) or transfected with IL-27 overexpression plasmids (IL-27over) for 48 hours was detected by FCM, and the ratios of p-STAT3 to STAT3 were calculated. (E and F) Expression of COX-2 in peripheral blood monocytes (pMos) (n = 12), eMφs (n = 12), and dMφs (n = 12) was analyzed by FCM. Statistical graph of (E) was shown in (F). (G) Expression of COX-2 in dMφs (n = 9) cocultured with Ctrl or FBP (0.5 mM for 24 hours)–treated ESCs was detected by FCM. (H) Expression of COX-2 in dMφs (n = 9) cocultured with FBP (0.5 mM for 24 hours)–pretreated ESCs or IL-27over ESCs for 48 hours was detected by FCM. Data were presented as means ± SEM or median and quartile and analyzed by t test, one-way ANOVA test, or Kruskal-Wallis test. *P < 0.05, **P < 0.01, and ***P < 0.001.