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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Semin Cancer Biol. 2017 Dec 2;54:121–130. doi: 10.1016/j.semcancer.2017.11.021

Figure 2. RAS signaling and tumorigenesis in response to inhibition of Galectins and mTOR.

Figure 2

a) HRAS-GAL1 and KRAS-GAL3 coupling support downstream RAS oncogenic signaling. b) Schematic of predicted effects of anti-Galectin treatments in H- and KRAS cancers. Galectin-1 inhibition using OTX008 or other GAL1 inhibitors results in loss of HRAS at the lipid ordered/disordered domain borders, and disruption of MAPK mitogenic signaling. GAL3 inhibition with modified citrus pectin, GSC-100, or other inhibitors blocks MAPK signaling by destabilizing KRAS membrane retention. Some PI3K signal output is retained by these treatments. c) Predicted effects of dual inhibition of Galectins and mTOR. Rapamycin or rapalog treatment potently reduces mTOR survival signaling. Combinatorial pathway inhibition blocks MAPK and PI3K signaling by RAS, resulting in an additive anti-tumor effect over either monotherapy.