Fig 2: Pre-neoplastic and neoplastic lesions positive for COX-2 immunoreactivity. (A) Chronic gastritis with plasmocytes; (B) Atrophic gastritis (atrophy); (C) Intestinal metaplasia; (D) Tumor

Fig 3: CDH1 or ZEB1 regulation modulates the susceptibility to sulfasalazine in vivo. (A–D) Representative images, weights, and immunoblotting of tumors grown in mice with HN9 cells transfected with CDH1 overexpression or control vector. The mice were subjected to vehicle or SAS (250 mg/kg daily per intraperitoneal route) for 21 days. Immunoblotting was performed from tumors extracted at 21 days with the primary antibodies of vimentin, ZEB1, PTGS2, 4HNE, E-cadherin, GSH, and ß-actin. (E–H) Representative images, weights, and immunoblotting of tumors harvested in mice HN4 cells with or without ZEB1 overexpression or control vector. The mice were also subjected to SAS or vehicle for 21 days. *P < 0.05, *P < 0.01, ***P < 0.001 between the vector control and CDH1 or ZEB1 overexpression or between vehicle or SAS treatment.

Fig 4: Cyclooxygenase-2 (COX-2) mRNA expression (A) and protein production (B, and C). COX-2 mRNA expression was determined by RT-PCR (A), and COX-2 protein production was determined using Western blot (B: representative immunoblot; C: protein expression calculated as Arbitrary Densitometric Units; A.D.U.) in the NCTC 2544 72 h after the addition of M. MeOH (50 µg/mL) with INF-? + H. * Significantly different than control; ° significantly different than INF-?/H-treated samples (p < 0.05).

Fig 5: The mRNA (A) and protein (B) expressions of COX-2 and iNOSin human oral squamous carcinoma HSC-3 cells. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. the control group. Geniposide-L: 25 µg/mL geniposide; LcS-geniposide-L: 1.0 × 106 CFU/mL LcS + 25 µg/mL geniposide; Geniposide-H: 50 µg/mL geniposide; LcS-geniposide-H: 1.0 × 106 CFU/mL LcS + 50 µg/mL geniposide.