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 4 Underlying mechanisms of ASAP3 in HGC-27 cells using transcriptome sequencing.
A: The principal component analysis of the short hairpin (sh)-negative control (NC)-HGC-27 and sh-ASAP3-HGC-27 cells; B: The volcano plot of the differential expressed messenger RNAs (DEMs) between the sh-NC-HGC-27 and sh-ASAP3-HGC-27 cells; C: The heatmap of the identified DEMs; D: The Gene Ontology terms enriched by the identified DEMs; E: Kyoto Encyclopedia of Genes and Genomes pathway analysis of the identified DEMs. PCA: Principal component analysis; PC: Principal component; GO: Gene Ontology; NADPH: Nicotinamide adenine dinucleotide phosphate hydrogen; KEGG: Kyoto Encyclopedia of Genes and Genomes; BP: Biological process; MF: Molecular function; CC: Cellular component; cAMP: Cyclic adenosine monophosphate; AGE-RAGE: Advanced glycation end products-receptor for advanced glycation end products; TNF: Tumor necrosis factor; FoxO: Forkhead box O; sh: Short hairpin; 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