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. 2026 Apr 8;12(15):eaec4368. doi: 10.1126/sciadv.aec4368

Fig. 3. SLC13A2 inhibits HCC progression in the mouse model induced by HTVi.

Fig. 3.

(A) Diagram showing LKO strategy and study design. (B) SLC13A2 KO efficiency in mouse liver tissues (n = 6). (C and D) Representative liver morphology and liver/body weight ratios (n = 16). Scale bar, 5 mm. (E) Tumor incidence and maximal tumor size (n = 13) in the two groups. (F) Liver and serum ALT/AST activity (n = 10). (G and H) Representative H&E staining and Ki67 staining showing tissue morphology and proliferation (n = 6). (I) Immunoblots of signaling pathways associated with tumor growth (n = 6). (J) Diagram of study design for the overexpression experiment. (K) SLC13A2 overexpression efficiency in mouse HCC tissues. (L and M) Representative liver morphology and liver/body weight ratios (n = 11 for the GFP group and n = 12 for the SLC13A2-OE group). Scale bar, 5 mm. (N) Tumor incidence (left) and the maximal tumor size (right, n = 11 for the GFP group and n = 10 for the SLC13A2-OE group) in the two groups. (O) Liver and serum ALT/AST activity (n = 11 for the GFP group and n = 10 for the SLC13A2-OE group). (P and Q). Representative H&E staining and Ki67 staining showing tissue morphology and proliferation (n = 6). (R) Immunoblots of signaling pathways associated with tumor growth (n = 6). The data are presented as means ± SEM. *P < 0.05; **P < 0.01, LKO versus Ctrl group, SLC13A2-OE versus GFP group, two-tailed unpaired Student’s t test.