Background: Epithelial-to-mesenchymal transition (EMT) is involved in tumor progression, invasion, migration and metastasis. EMT is a process by which polarized epithelial cells acquire motile mesothelial phenotypic features. This process is initiated by disassembly of cell-cell contacts through the loss of epithelial markers and replacement of these markers by mesenchymal markers. Reconstruction of the cytoskeleton and degradation of the tumor basement membrane ensures the spread of invasive malignant tumor cells to distant locations. Accumulating evidence indicates that curcumin, as a well-known phytochemical, can inhibit EMT/metastasis through various mechanisms and pathways in human tumors.
Conclusions: In this review, we summarize the mechanisms by which curcumin may affect EMT in cells under pathological conditions to understand its potential as a novel anti-tumor agent. Curcumin can exert chemo-preventive effects by inhibition and reversal of the EMT process through both TGF-β-dependent (e.g. in hepatoma and retinal pigment epithelial cancer) and -independent (e.g. in oral cancer, colorectal cancer, pancreatic cancer, hepatocellular carcinoma, breast cancer, melanoma, prostate cancer, bladder cancer, thyroid cancer and lung cancer) pathways. Curcumin can also mitigate chemoresistance through EMT suppression and promotion of the antiproliferative effects of conventional chemotherapeutics. Therefore, curcumin has the potential to be used as a novel adjunctive agent to prevent tumor metastasis, which may at least partly be attributed to its hampering of the EMT process.
Keywords: E-cadherin; Smad pathway; TGF-β; Turmeric, Curcumin; Vimentin.