Fig 2: The effect of C-1 on tumor growth in a xenograft mouse model of CRC.(A) Images of dissected tumors from mice treated with vehicle (n = 7) or C-1 (n = 7) via intraperitoneal injections. (B and C) Tumor weight and tumor volume of mice treated with vehicle (n = 7) or C-1 (n = 7) via intraperitoneal injections. Error bars represent means ± SD. (D) Images of subcutaneous tumors, taken on day 20 of the study, from mice treated with vehicle (n = 7) or C-1 (n = 7) via intratumoral injections. (E) Body weight (top) and tumor volume (bottom) of mice treated with vehicle (n = 7) or C-1 treated (n = 7) via intratumoral injections. Error bars represent means ± SD. (F and G) Tumor weight and tumor GFP fluorescence measurements recorded from mice treated with vehicle (n = 7) or C-1 (n = 7), via intratumoral injections. Error bars represent means ± SD. (H) GFP fluorescence images of intratumoral vehicle and C-1–treated mice taken on day 20. (I) Representative hematoxylin and eosin (H&E) and IHC stains of AXIN2, CD44, Ki-67, cleaved caspase-3, CD31, and CD163 in tumor tissue from intratumoral vehicle- and C-1–treated mice. Scale bars, 50 µm. (J) Quantification of AXIN2, CD44, Ki-67, CD31, cleaved caspase-3, and CD163 immunostains in the tumors of intratumoral vehicle- and C-1–treated mice. Plots represent individual data points with error bars representing means ± SD. *P > 0.05 and ***P > 0.001.

Fig 3: CD31+ staining at the irradiation sites of murine brain, lung and colon tissue (A). Scale bar, 100 µm. Quantitation of five high power fields for each murine tissue (N = 6 per time point; B). Data are expressed as mean ± SEM per high power field. ap < 0.05 vs. IgGa, bp < 0.05 vs. IgG2a + RT by Tukey's multiple comparison test.

Fig 4: Changes of portal vessels, central vessels, and sinusoid at different time points during liver fibrogenesis. (A) C57BL/6J mice were injected with CCl4 to induce fibrosis. Harvested liver tissues at different time points were processed for immunofluorescence staining for GS (pericentral area marker) and CD31 (endothelial marker). Slides were counterstained with DAPI. Arrows, portal vessels; arrowheads, central vessels. Scale bar, 100 µm. (B) The number of CD31-positive vessels in the periportal area was measured. (C) The number of CD31-positive vessels in the pericentral area was measured. (D) C57BL/6J mice were injected with CCl4 to induce fibrosis. Harvested liver tissues at different time points were processed for immunohistochemistry staining for LYVE1 (LSEC marker). Scale bar, 100 µm. (E) LYVE1-positive area was analyzed by ImageJ. (F) Quantitative real-time PCR was used to analyze the mRNA levels of CD34. (G) C57BL/6J mice were injected with CCl4 to induce fibrosis. Harvested liver tissues at different time points were stained using sirius red for fibrosis analysis. Scale bar, 200 µm. (H) Sirius red–positive area was analyzed by ImageJ. n = 5/group. Mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Fig 5: The expression of major metabolite transporters does not differ, except for CPT1a in breast tumors of obese and lean mice. (A–G): E0771 cell line; sample size: n = 7 for ND except (A) (lost sample), (F) (Grubb’s outlier) n = 6 and n = 8 for HFD. (H–N): PY8119 cell line; sample size: n = 8 for ND and n = 8 for HFD. (A,H) IHC staining for CD31 expression, scale bar = 100 µm. (B,I) IHC staining for GLUT1. (C,J) IHC staining for MCT1. (D,K) IHC staining for MCT4. (E,L) IHC staining for CA9. (F,M) IHC staining for CD36. (G,N) IHC staining for CPT1a. All scale bars except for CD31 = 50 µm. Statistical analyses: unpaired t-test; ns p > 0.05; * p < 0.05.