Fig 2: A Tumor volume of different mice. B IHC for ASCL2 and ki-67 index (× 400). C TUNEL-DAPI staining (× 400) and D TUNEL ( +) cell assay. E CEA, CA199, and c-Met expressed and F quantificated (sh-ASCL2 vs. other groups, n = 6, *P < 0.05)

Fig 3: A Tumor volume in the Con, sh-TMED2, and control-shTMED2 mice after 28 days. B IHC for TMED2 and determination of the Ki-67 index. C TUNEL-DAPI staining assay (× 400) and D quantification of TUNEL(+) cells. E Western blot assay of CEA, NSE, and EGFR expression in vivo. F Quantification of TMED2, CEA, NSE, and EGFR expression. Protein levels were normalized to β-actin. (sh-TMED2 vs. other groups, *P < 0.05, n = 6 per group)

Fig 4: A Proliferation assay of the Con, sh-TMED2, and control-shTMED2 group after 4 days of treatment. B PI-Hoechst staining assay (× 800) and C quantification of PI(+) cells. D Western blot assay of TMED2, CEA, NSE, and EGFR expression in vitro. E Quantification of CEA, NSE, and EGFR expression. Protein levels were normalized to β-actin. (sh-TMED2 vs. other groups, *P < 0.05, n = 6 per group)

Fig 5: Transcriptome analysis and histopathologic characteristics between GC organoids and their derived primary GCs(A) Heatmap of differentially expressed genes and (B) pathways between organoids and their corresponding tumor tissue. The colored bar represents the log2-transformed values. Differentially expressed genes (p < 0.05, log2 (fold change) > 1) of organoids and tissue are indicated in red or blue, respectively.(C) Representative images of bright-field microscopy, hematoxylin and eosin staining of GC organoids, and matched primary GC tumor tissues.(D) Immunohistochemistry of GC protein markers CK7 and CEA in organoids and their corresponding primary GC tumor tissues. Scale bar, 50 μm.