Curcumin (diferuloylmethane) is bioactive phenolic compound which exerts diverse antimetastatic effect. Several studies have reported the antimetastatic effect of curcumin by its ability to modulate the epithelial-to-mesenchymal transition (EMT) process in different cancers, but underlying molecular mechanism is poorly understood. EMT is a highly conserved biological process in which epithelial cells acquire mesenchymal-like characteristics by losing their cell-cell junctions and polarity. As a consequence, deviation in cellular mechanism leads to cancer metastasis and thereby death. In this perspective, we explored the antimetastatic potential and mechanism of curcumin on the EMT process by establishing in vitro EMT model in lungs cancer (A549) cells induced by TGF-β1. Our results showed that curcumin mitigates EMT by regulating the expression of crucial mesenchymal markers such as MMP2, vimentin and N-cadherin. Besides, the transcriptional analysis revealed that the curcumin treatment differentially regulated the expression of 75 genes in NanoString nCounter platform. Further protein-protein interaction network and clusters analysis of differentially expressed genes revealed their involvement in essential biological processes that plays a key role during EMT transition. Altogether, the study provides a comprehensive overview of the antimetastatic potential of curcumin in TGF-β1-induced EMT in lung cancer cells.
Supplementary information: The online version contains supplementary material available at 10.1007/s13205-022-03360-7.
Keywords: Curcumin; EMT; Metastasis; NanoString; PPI; PanCancer; TGF-β.
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