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. 2023 Nov 10;42:297. doi: 10.1186/s13046-023-02870-3

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — CXCR7 activates YAP through the Gα_q/11-ROCK-LATS axis in gastric cancer. A, B CXCR7 activation induced YAP dephosphorylation through Gaq/11. MGC803 and Hs746T cells were transiently transfected with control, Ga_q/11, or Ga_s siRNAs. MGC803 and Hs746T cells were treated with TC. YAP, phosphorylated YAP, Ga_q/11 and Ga_s were determined by immunoblotting. C CXCR7 activation induces YAP nuclear localization through Ga_q/11. MGC803 cells were transiently transfected with control, Ga_q/11 or Ga_s siRNAs. MGC803 cells were treated with TC. Endogenous YAP (green) and nuclei (blue) were stained with specific antibodies and DAPI, respectively; scale bar, 20 mm. Quantifications of YAP subcellular localization from at least 100 randomly selected cells. C, cytoplasm; N, nucleus. D Nucleoplasm separation experiments by immunoblotting confirmed that Gα_q/11 silencing could block the YAP nuclear accumulation caused by CXCR7 activation in MGC 803 cells. E CXCR7 activation via TC decreases LATS1 activity. MGC803 and Hs746T cells were stimulated with TC. LATS1 was immunoprecipitated. Phosphorylation of YAP by LATS1 was determined by a phospho-YAP antibody. F Ectopic expression of LATS1 blocks YAP dephosphorylation induced by CXCR activation. MGC803 and Hs746T cells were transiently transfected with control, LATS1 wild type (WT), or kinase dead mutant (K/R). MGC803 and Hs746T cells were treated with TC for 1 h. Phosphorylation and protein levels of YAP were determined by immunoblotting. G Rho GTPase is involved in YAP dephosphorylation induced by CXCR activation. MGC803 and Hs746T cells were transiently transfected with control, Myc-Rho-L63, or C3. MGC803 and Hs746T cells were treated with TC. Total YAP and phosphorylated YAP protein levels were determined by immunoblotting. H ROCK is required for CXCR7-induced YAP activation. Serum-starved MGC803 and Hs746T cells were pretreated with GSK429286 (1 mmol/L) or Y27632 (1 mmol/L) for 4 h, followed by treatment with TC. Total YAP and phosphorylated YAP protein levels were determined by immunoblotting