Title : Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3.

Pub. Date : 2014 May

PMID : 24668500






4 Functional Relationships(s)
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1 Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, alpha9 nicotinic acetylcholine receptor and STAT3. Nicotine signal transducer and activator of transcription 3 Homo sapiens
2 Nicotine-induced up regulation of galectin-3 is due to an increased expression of alpha9 isoform of nicotinic acetylcholine receptor (alpha9nAChR), which activates transcription factor STAT3 that in turn, physically binds to galectin-3 (LGALS3) promoter and induces transcription of galectin-3. Nicotine signal transducer and activator of transcription 3 Homo sapiens
3 Moreover, nicotine-induced enrichment of side population cells with cancer stem cell-like properties was modulated by galectin-3 expression and could be significantly reduced by transient knock down of LGALS3 and its upstream signaling molecules STAT3 and alpha9nAChR. Nicotine signal transducer and activator of transcription 3 Homo sapiens
4 Thus, galectin-3 or its upstream signaling molecule STAT3 or alpha9nAChR could be a potential target to prevent nicotine-induced chemoresistance in breast cancer. Nicotine signal transducer and activator of transcription 3 Homo sapiens