Background and objectives: Sulindac exerts antineoplastic effects in various malignant neoplasms, including oral squamous cell carcinoma (OSCC) cell lines. Our purpose was to explore sulindac effects in the hamster’s cheek pouch oral carcinogenesis model (HOCM).
Methods: Thirty healthy Syrian golden hamster’s were divided in 3 experimental groups (A1, A2, B) and 2 control groups (C1, C2) ( n = 6 each). All animals’ right buccal pouches were treated with 0.5% DMBA for 9 (A1, C1) or 14 (A2, B, C2) weeks and were subsequently sacrificed. The animals of groups A1 and A2 received sulindac from start and group B from 10th week. Groups C1 and C2 did not receive sulindac. Treated buccal pouches were removed and examined macroscopically, histopathologically and immunohistochemically for Ki-67, phospho-Stat3 (Tyr705) and Survivin.
Results: Tumour volume and the proportion of animals developing OSCC was significantly lower in group A2 compared to C2 ( p < 0.05). OSCC developing in groups A2 and B were better differentiated compared to C2 ( p < 0.05). Groups A1 and C1 developed epithelial dysplasia, which was less severe in A1 compared to C1 ( p < 0.05). Ki-67 positivity was significantly higher in group C2 compared to B and in C1 compared to A1 ( p < 0.05). Survivin positivity was significantly higher in group C2 compared to group B and A2 and in group C1 compared to group A1 ( p < 0.05). All tumours in groups A1, A2, B and C1 were negative for phospho-Stat3 while half tumours in group C2 showed positivity.
Conclusions: Sulindac appears to partially prevent the transformation from oral premalignant lesions to OSCC. Sulindac appears to decrease the rate of cell proliferation as exerted by Ki-67 positivity and to prevent the expression of Survivin and phospho-Stat3 in the HOCM, thus playing a potential role in chemoprevention and treatment of OSCC.
Key words: sulindac; squamous cell carcinoma; antineoplastic effects; hamster’s carcinogenesis model