In breast cancer cells, the survival signaling molecules, such as NF-B, produce a consequences a pivotal role in cell proliferation44 (Fig. 2). Liu et al. reported that curcumin was sprightly to inhibit NF-B expression45 and toggled many downstream signaling pathways, which silenced inflammatory cytokines, such as CXCL1 and CXCL2, and mediated the aeration of matrix metalloproteinase 9 (MMP-9), urokinase plasminogen activator (uPA), uPA receptor (uPAR), intercellular adhesion molecule 1 (ICAM-1), and chemokine receptor 4 (CXCR4). Therefore, curcumin is believed to perform its impact regarding cell accrual and ill feeling of breast cancer partially through the downregulation of NF-B signaling pathways.

Hormone factors plus contribute to the enhancement and proliferation of breast cancer cells. HER2 and estrogen are the typical targets belonging to this category. Yim-im et al. found that a combination of curcumin and its analogues AS-KTC006 and AS-KTC021 could inhibit one specific tyrosine kinase and take steps as a challenger adjoining HER2. Furthermore, curcumin can add occurring the doxorubicin (a chemotherapeutic drug) cytotoxicity by decreasing redundancy HER2 in breast cancer cells. On the new hand, immunoliposome encapsulation is believed to put in curcumin selectivity in breast cancer cells that overexpress HER2.50 Recent research proved that curcumin, acting as a phytoestrogen, competitively inhibited endogenous estrogen, which furthermore contributed to the suppression of breast cancer cell calculation.

Furthermore, curcumin suppresses breast cancer proliferation partially due to accumulation trophic signaling pathways. Curcumin showed its influence upon fatty rancorous synthase (FASN) and acetyl-CoA carboxylase (ACC) through AMPK activation. Curcumin as well as partially inhibited breast cancercell accretion by downregulating the insulin-later stock factor 1 (IGF-1) axis. Results from Thulasiraman et al. demonstrated that curcumin mediated the suppression of the fatty cuttingbinding protein 5 (FABP5)/peroxisome proliferatoractivated receptor / (PPAR/) alleyway by making breast cancer cells more throbbing to retinotic unpleasant. The associated matter is applicable to leptin and its receptor.