Figure 1.
(a) Tumour necrosis factor alpha (TNFα) stimulated cyclooxygenase‐2 (COX‐2) mRNA in Normal fibroblast (NFs) and cancer‐associated fibroblasts (CAFs). NFs or CAFs were cultured in medium with or without TNFα (10 ng/ml). Stimulation by TNFα elicited 10‐fold upregulation of COX‐2 mRNA in NFs, compared to 7‐fold upregulation of COX‐2 mRNA in CAFs (n = 4, *P < 0.05 and **P < 0.01, respectively). Level of COX‐2 in resting CAFs was 6‐fold higher than that in resting NFs (n = 4, #P < 0.05), while level of COX‐2 in TNFα‐stimulated CAFs was 4‐fold higher than that in TNFα‐stimulated NFs (n = 4, #P < 0.05). (b) TNF α induced COX ‐2 protein expression in NF s and CAF s. NFs or CAFs were cultured in medium with or without TNFα (10 ng/ml). Stimulation by TNFα elicited 3‐fold upregulation of COX‐2 protein in NFs, but 2‐fold upregulation of COX‐2 protein in CAFs (n = 4, *P < 0.05). Level of COX‐2 protein in resting CAFs was 3‐fold greater that in resting NFs (n = 4, #P < 0.05), while level of COX‐2 protein in TNFα‐stimulated CAFs was 2‐fold greater than that in TNFα‐stimulated NFs (n = 4, #P < 0.05). (c) TNF α increased synthesis of PGE 2 in NF s and CAF s. NFs or CAFs were cultured in medium with or without TNFα (10 ng/ml). Stimulation by TNFα elicited 13‐fold upregulation of PGE 2 synthesis in NFs compared to 6‐fold upregulation of synthesis in CAFs (n = 4, *P < 0.05 and **P < 0.01 respectively). Level of COX‐2 protein in resting CAFs was 7‐fold greater than that in resting NFs (n = 4, #P < 0.05), while level of COX‐2 protein in TNFα‐stimulated CAFs was 4‐fold greater than that in TNFα‐stimulated NFs (n = 4, #P < 0.05).