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. 2020 Mar 17;6:14. doi: 10.1038/s41420-020-0249-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Cancer cell-produced TRAIL can bin TRAIL-R2 leading to autocrine cell-autonomous stimulation of Rac1-dependent migration. This signal is independent of the death domain (DD) but requires the membrane-proximal domain (MPD) of TRAIL-R2. Rac1 activity is normally inhibited by ROCK. Upon oncogenic activation of KRAS, KRAS inhibits ROCK, thereby releasing Rac1 to be fully activated by TRAIL-R2.