Figure 10.

An emerging functional relationship between cytokine production, autophagy and inflammation in the tumor microenvironment. Co-culture of fibroblasts with cancer cells drives the onset of oxidative stress and NFκB-activation in cancer-associated fibroblasts.²,³ Here, we show that one of the consequences of this reciprocal interaction, between fibroblasts and cancer cells, is elevated cytokine production, which may drive both autophagy and inflammation in the tumor microenvironment. Autophagy in cancer-associated fibroblasts destroys Cav-1 (via lysosomal degradation),¹ further driving oxidative stress and NFκB activation (marked by the large red arrow). Importantly, transient knock-down of Cav-1 in fibroblasts, using an siRNA approach, is sufficient to induce the onset of oxidative stress and autophagy, as well as NFκB activation.²,³