Research Paper Volume 13, Issue 12 pp 16178—16197

GPR30-mediated HMGB1 upregulation in CAFs induces autophagy and tamoxifen resistance in ERα-positive breast cancer cells

A working model of GPR30-mediated paracrine effects of HMGB1 on autophagy in CAFs and cancer cells. G1 stimulation can promote GPR30-induced secretion of HMGB1 by cancer cells; this was proved to be dependent on the PI3K/AKT signaling pathway in CAFs. The elevated HMGB1 induced autophagy, while suppressing apoptosis through MEK/ERK under exposure to tamoxifen.

Figure 7. A working model of GPR30-mediated paracrine effects of HMGB1 on autophagy in CAFs and cancer cells. G1 stimulation can promote GPR30-induced secretion of HMGB1 by cancer cells; this was proved to be dependent on the PI3K/AKT signaling pathway in CAFs. The elevated HMGB1 induced autophagy, while suppressing apoptosis through MEK/ERK under exposure to tamoxifen.