Copyright: ©Author(s) 2026.
World J Gastrointest Oncol. Aug 15, 2026; 18(8): 117876
Published online Aug 15, 2026. doi: 10.4251/wjgo.v18.i8.117876
Published online Aug 15, 2026. doi: 10.4251/wjgo.v18.i8.117876
Figure 7 Underlying mechanisms of ASAP3 in AGS cells using proteomics.
A: The principal component analysis of the over-expression (oe)-negative control (NC)-AGS and oe-ASAP3-AGS cells; B: The volcano plot of the differential expressed proteins (DEPs) between the oe-NC-AGS and oe-ASAP3-AGS cells; C: The heatmap of the identified DEPs; D: Subcellular localization analysis of the DEPs; E: The Gene Ontology terms enriched by the identified DEPs, including biological process, cellular component, and molecular function; F: Kyoto Encyclopedia of Genes and Genomes pathway analysis of the identified DEPs. PC: Principal component; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; BP: Biological process; MF: Molecular function; CC: Cellular component; oe: Over-expression; NC: Negative control.
- Citation: Huang XB, Deng Y, Gong SY, Yu M, Cai H. ASAP3 disrupts ASAP1-ARHGAP12 to inhibit RhoA and yes-associated protein/transcriptional coactivator with PDZ-binding motif, suppressing gastric cancer progression. World J Gastrointest Oncol 2026; 18(8): 117876
- URL: https://www.wjgnet.com/1948-5204/full/v18/i8/117876.htm
- DOI: https://dx.doi.org/10.4251/wjgo.v18.i8.117876