Table 4 Resveratrol and its associated assessments as analysed in the selected papers
Author | Carcinogen assessed | Exposure compounds | Action mechanism | Observation inferred |
|---|---|---|---|---|
Berta et al. [9] | DMBA | Resveratrol | Decrease in neoplastic proliferation | Resveratrol formulas were non-toxic and stopped the emergence and development of OSCC |
Masuelli et al. [10] | HNSCC | Resveratrol and curcumin | Decrease in ROS, NF-B, pAKT, LC3-II, PARP-1 and Bax/Bcl-2 ratio and decrease in p-ERK2 | Curcumin and resveratrol together were more successful in preventing neoplastic development than curcumin treatment alone |
Pradhan et al. [11] | CSCs (H-357) | Resveratrol | Decrease in neoplastic proliferation, metastatic and angiogenic biomarkers | Resveratrol inhibited CSC spread, expansion and differentiation by lowering the number of cytokines in CSC-infused cells |
Shrotriya et al. [12] | 4NQO | Resveratrol and GSE | Decrease in size of neoplastic tissue diameter, expansion and severity of the neoplastic growth | GSE and resveratrol, the two evaluated drugs, were associated with lower proliferation and oral tumour development, consequently suppressing proliferation and promoting apoptosis and autophagy |
Uzawa et al. [13] | OSCC | Cetuximab and resveratrol | Decrease in neoplastic proliferation, integrin β1 and uPAR levels | Resveratrol reduced the expression of the uPAR and, as a result, the signalling molecules that were downward of the EGFR |