Colorectal Carcinoma Growth Inhibition by Curcumin Via Targeting NRP2, N-Cadherin, and Vimentin Expression

The present study investigated the effect of curcumin on colorectal carcinoma cells and explored the underlying mechanism. In the present study curcumin treatment caused a dose-dependent suppression in the viability of DLD1 and HT29 CRC cells. However, no changes were observed in the viability of CRL-1831 cells on treatment with various concentrations of curcumin. Curcumin treatment also caused a significant decrease the colony forming potential of DLD1 and HT29 CRC cells. It was found that curcumin treatment at 16 mu M concentration didn't affect the colony forming potential of CRL-1831 cells. It was observed that curcumin treatment at 16 mu M concentration markedly reduced the invasion potential of DLD1 and HT29 cells. The decrease in invasion potential by 16 mu M curcumin treatment was higher in HT29 cells compared to DLD1 cells. Curcumin treatment also led to a marked reduction in the expression of NRP2 protein in DLD1 cells and HT29 cells. Western blotting data also showed that curcumin treatment at 16 mu M concentration effectively increased the expression of E-cadherin and suppressed the level of N-cadherin & Vimentin in DLD1 cells and HT29 cells. In summary, curcumin treatment suppresses the viability and invasion potential of colorectal carcinoma cells without affecting the normal colonic cells. Moreover, it targets the expression of NRP2 protein, promotes E-cadherin expression, and downregulates the expression of N-cadherin and Vimentin in DLD1 and HT29 CRC cells. Therefore, curcumin can be investigated further as a therapeutic candidate for the treatment of colorectal cancer.