Surely, the treatment of cancer cells with IGF-1 ligand would positively affect NFkB signaling pathway, however, there would be a long way between IGF1/IGF1R signaling pathway and NFkB survival/ proliferative signal. Once the ligand binds to the receptor, IGF1R activates the several downstream target molecules composed of PLCr, MAPK, and PI3K/Akt, all of which contribute to the enhanced cellular viability. In contrast, NFkB signal is activated by numerous causes; the activation of Toll-like or TNF receptor, the change in stability of TRAF6, the susceptibility to the ubiquitin-proteasome26S dependent degradation of IkB, etc. Collectively, I would like to emphasize again that you would easily find the molecular change in NFkB signaling pathway, but to uncover the cross-talk of NFkB with IGF1 signal would be challenging considering the chaotic molecular pathways revealed up to now.

Thank u Yoshida but ...

What is about the crosstalk between TGF-beta and estrogen?

Thank you...

I want to know this cross talk in breast cancer cells (epithelial cells).