sulphoraphane shown to arrest fat cell growth. Sulphoraphane decreased PPAR-gamma and C/EBP-alpha expression as well as suppressing the cell growth cycle. Obvious implications in weight loss
cancer stem cells may also contribute to tumor formation, metastasis, and treatment resistance
Studies have shown that some agents (such as metformin) can selectively target cancer stem cells and that dietary polyphenols, curcumin, peperine, and sulforaphane, which are derived from broccoli/broccoli sprouts, are able to target breast cancer stem cells via inhibition of the Wnt signaling, which affects mammosphere size and colony formation
niclosamide inhibits tumor growth and reduces tumor weight
Niclosamide treatment inhibited the expression of cyclin D1, Hes1, and PTCH by 33%, 57%, and 79%, respectively
The mechanism via which niclosamide, a protonophoric anthelmintic drug, induces stem-like-cell-specific toxicity in breast cancer is interesting. It is an old drug that has been used to treat tapeworms in animals
Niclosamide is known to uncouple mitochondrial oxidative phosphorylation during tapeworm killing
A screening of autophagy modulators revealed that niclosamide is a novel inhibitor of mTORC1 signaling
A recent work also demonstrated that niclosamide induces the apoptosis of myelogenous leukemic cells via the inactivation of NF-kappaB and reactive oxygen species generation
Niclosamide was also reported to inhibit Wnt signaling [31]–[33] in colon cancer cells
Our recent work demonstrated that niclosamide disrupts multiple metabolic pathways in ovarian-cancer-initiating cells
The present study showed that niclosamide treatment resulted in the downregulation of target genes involved in the self-renewal of cancer stem-like cells and inhibited breast SPS