Curcumin could assist as a chemosensitizer for new anticancer agents in treating human breast cancer cells, especially multi-drug-resistant (MDR) breast cancer cells. Limtrakul et al. investigated the effects of tetrahydrocurcumin almost three ATP-binding record (ABC) drug transporters, including P-glycoprotein (ABCB1/P-gp), multidrug resistance protein 1 (ABCC1), and mitoxantrone resistance protein (ABCG2/MXR). The results illustrated that in a combination-dependent environment, P-gp ATPase upheaval is stimulated and [(125)I]-iodoarylazidoprazosin (IAAP) is inhibited. Thus, the binding of MDR later IAAP leads to the efflux of mitoxantrone and the inhibition of pheophorbide. Curcumin also exerts antique modification of relevant gene transcription, such as downregulation of Bcl-2 and inhibition of apoptosis proteins (IAPs) in MCF-7R cells taking into consideration overexpression of P-gp. In 5-FU-resistant cells, curcumin acts as a chemosensitizer for 5-FU by silencing the enzyme thymidylate synthase (TS) in breast cancer cells. TS, an upstream molecule of NF-B, can be inhibited by 5-FU. However, prolonged drying of 5-FU reversely increases the freshening of TS and activates TS-dependent NF-B, which causes 5-FU resistance in breast cancer cells. Curcumin can silence TS and suppress NF-B, and consequently chemosensitize the 5-FU anticancer go-getter. A linked mechanism can be found in doxorubicin-resistant breast cancer cells. Meiyanto et al.s psychiatry suggested thatcurcumin inactivated NF-B and condensed the ventilation of HER2 in doxorubicin-resistant breast cancer cells