Spatial transcriptomics reveals tumor niche heterogeneity in advanced gastric cancer and suggests a tumor-promoting role for KRT6B

Figure 6 KRT6B is upregulated in gastric cancer, correlates with poor prognosis, and promotes malignant phenotypes in vitro. A: Representative immunohistochemical staining images showing KRT6B expression in gastric cancer tissues and matched adjacent non-tumor tissues (scale bar, 200 μm); B: Quantification of KRT6B immunohistochemistry scores (H-score) in paired tumor and adjacent non-tumor tissues; C: Analysis of UCSC Xena-integrated TCGA-STAD and GTEx transcriptomic data showing significantly increased KRT6B mRNA expression in gastric cancer tissues compared with normal gastric tissues; D: Kaplan-Meier overall survival analysis of patients stratified by KRT6B expression level; E: Western blot validation of stable KRT6B overexpression in AGS and SNU-601 cells (GAPDH as a loading control); F and G: CCK-8 assays showing increased proliferative capacity in KRT6B-overexpressing AGS (F) and SNU-601 (G) cells; H and I: Representative flow cytometry histograms of EdU incorporation in AGS (H) and SNU-601 (I) cells. A no-EdU control was used to define the APC-positive gate; J and K: Quantification of EdU-positive cell proportions in AGS (J) and SNU-601 (K) cells; L and M: Representative Transwell invasion assay images of AGS (L) and SNU-601 (M) cells; N and O: Quantification of invading cell numbers in AGS (N) and SNU-601 (O) cells; P and Q: Representative wound-healing assay images (0 hour and 24 hours) of AGS (P) and SNU-601 (Q) cells; R and S: Quantification of wound closure rates in AGS (R) and SNU-601 (S) cells. Data are presented as mean ± SD from independent experiments. NS: Not significant; ^aP < 0.05, ^bP < 0.01, ^cP < 0.001.